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35 publications mentioning rno-mir-212

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-212. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 215
Indeed, miR-212 expression is deregulated in various cancers and its expression has been correlated to disease progression. [score:8]
In addition, miR-212 expression can be regulated by various hormones, adding another layer of complexity to their regulation and role in development and disease (Godoy et al., 2011). [score:8]
In pancreatic carcinomas it has been shown that miR-212 targets the tumor suppressor retinoblastoma (Rb1) (Park et al., 2011), whereas the methyl binding protein (MeCP2) seems to be the main target in some of the gastric tumors (Wada et al., 2010). [score:7]
Specifically, we found that rats with extended access to cocaine showed increased expression of the CREB-responsive gene Nurr1, and that expression levels were greatly increased by miR-212 overexpression in striatum (Hollander et al., 2010). [score:7]
These findings are consistent with an inhibitory effect of MeCP2 on miR-212 expression, suggesting that MeCP2 acts as a pro-addiction transcriptional repressor that, by attenuating miR-212 expression in response to cocaine, increases vulnerability to addiction. [score:7]
In the first study, smRNAs deep sequencing analysis in vascular smooth muscle cells show that the miR-132/miR-212 cluster is induced by the hormone angiotensin II and by targeting PTEN, increases the expression of the gene MCP1 (Monocyte chemotactic protein 1), a key regulator of cardiovascular disorders (Jin et al., 2012). [score:6]
We observed that virus -mediated MeCP2 knockdown or miR-212 expression (which decreases MeCP2 levels) in striatum reduced BDNF expression. [score:6]
miR-212 is downregulated and suppresses methyl-CpG -binding protein MeCP2 in human gastric cancer. [score:6]
miR-132 and miR-212 are increased in pancreatic cancer and target the retinoblastoma tumor suppressor. [score:5]
Incoronato et al. showed that miR-212 targets phosphoprotein enriched in diabetes (PED), a wide spectrum anti-apoptotic protein, and thereby plays an important role in tumor suppression (Incoronato et al., 2010). [score:5]
It is known that CRTC overexpression increases CREB activity and that miR-212 increases CRTC1 expression (Hollander et al., 2010). [score:5]
Similarly, pharmacologically induced disruption of DNA methyltransferase activity, which would be expected to attenuate the inhibitory activity of MeCP2 on gene expression, also increased miR-212/132 levels. [score:5]
Based on these observations, we hypothesized that in addition to the inhibitory effects of MeCP2 on miR-212 expression described above, MeCP2 levels in turn may be repressed by miR-212. [score:5]
Consistent with this hypothesis, we found that miR-212 overexpression profoundly decreased MeCP2 expression in cultured cells and in the striatum in vivo (Im et al., 2010). [score:5]
Further, lentivirus -mediated overexpression of miR-212 in the dorsal striatum resulted in a remarkable decrease in cocaine intake in the extended access rats compared to vector control, but overexpression did not alter cocaine intake in rats with restricted drug access (Figure 2). [score:4]
More importantly, disruption of striatal miR-212 signaling, achieved by striatal infusion of an antisense oligonucleotide, reversed the inhibitory effects of MeCP2 knockdown on cocaine intake in extended access rats (Im et al., 2010). [score:4]
Epigenetic regulation of miR-212 expression in lung cancer. [score:4]
As noted above, expression of miR-212 is regulated by CREB. [score:4]
Knockdown of striatal MeCP2 dramatically increased the stimulatory effects of self-administered cocaine on striatal miR-212 expression in rats with extended but not restricted access to the drug. [score:4]
Consistent with this hypothesis, in vitro studies showed that knockdown of MeCP2 increased miR-212 (and miR-132) expression in cultured cells (Im et al., 2010). [score:4]
Based on these observations, we hypothesized that MeCP2 may regulate baseline and cocaine -induced changes in miR-212 expression in striatum and thereby influence cocaine-taking behavior. [score:4]
Finally, computational and biochemical analysis showed that Sprouty-related EVH1 domain-containing protein 1 (SPRED1), a known negative regulator of Raf1 signaling, is a miR-212 target mRNA transcript and SPRED1 repression by miR-212 contributes to its stimulatory effects on Raf1 and CREB activity (Hollander et al., 2010). [score:4]
As CREB overexpression in ventral striatum is known to diminish the motivational properties of cocaine (Carlezon et al., 1998), we tested the hypothesis that miR-212 may regulate cocaine intake in extended access rats by amplifying striatal CREB activity through positive feedback mechanisms. [score:4]
These findings suggest that miR-212-MeCP2 interactions may determine expression levels of BDNF in striatum, which in turn regulates the motivational properties of cocaine. [score:4]
In a follow up study the same group also demonstrated that the expression on miR-212 in lung carcinomas is regulated by histone modifications (Incoronato et al., 2011). [score:4]
In other words, miR-212 and MeCP2 may be locked in a homeostatic relationship that serves to control miR-212 expression level and thereby influence vulnerability to cocaine addiction. [score:3]
Since miR-212 and miR-132 share the same seed region it is wi dely believed that they target the same mRNAs. [score:3]
Studies from Turrini et al. reveal that miR-212 may mediate drug resistance by targeting the ABC efflux transporter (Turrini et al., 2012). [score:3]
MicroRNA profiling in K-562 cells under imatinib treatment: influence of miR-212 and miR-328 on ABCG2 expression. [score:3]
miR-212 increases tumor necrosis factor-related apoptosis-inducing ligand sensitivity in non-small cell lung cancer by targeting the antiapoptotic protein PED. [score:3]
Figure 2 Overexpression of miR-212 in striatum reverses the motivational properties of cocaine in rats with extended but not restricted access to cocaine. [score:3]
To investigate the functional relevance of miR-212 -induced amplification of CREB activity in vivo on the suppressive effects of this miRNA on cocaine intake, we examined the effects of overexpressing the CREB co-activator CRTC1 (TORC1) on cocaine intake in rats with restricted or extended cocaine access. [score:3]
MeCP2 controls BDNF expression and cocaine intake through homeostatic interactions with microRNA-212. [score:3]
However, only a few putative miR-212/132 targets have been verified experimentally, which include MeCP2, Rb1and HB-EGF. [score:3]
Moreover, these findings provide compelling support for a key role for miR-212 in regulating the development of compulsive drug taking in rats, and perhaps in influencing vulnerability to cocaine addiction in human drug users. [score:3]
Considering that miR-212 expression levels may play a key role in regulating vulnerability to cocaine addiction, we next investigated the mechanisms by which baseline and cocaine -induced increases in striatal miR-212 levels are regulated. [score:3]
Conversely, inhibition of miR-212 signaling in the striatum, achieved by infusion of an antisense oligonucleotide, dramatically increased the motivational properties of cocaine in rats with extended, but not restricted, access to the drug (Figure 2). [score:3]
These data suggest that intrinsic or drug-induce alterations in the expression or activity of striatal miR-212 may influence vulnerability to addiction in human cocaine users. [score:3]
Furthermore, forskolin-stimulated expression of the CREB-responsive gene fos was also increased by miR-212, as was the activity of a luciferase -based CREB reporter construct (CRE-containing element from promoter of EVX-1). [score:3]
Interestingly, sequence analysis of the miR-212/132 gene cluster reveals that it is located in a CpG enriched region, which can serve as substrate for DNA methylation and gene regulation. [score:2]
Gonadotropin-releasing hormone induces miR-132 and miR-212 to regulate cellular morphology and migration in immortalized LbetaT2 pituitary gonadotrope cells. [score:2]
The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy. [score:2]
Role for BDNF in Regulating the Actions of Striatal miR-212 on Cocaine Intake. [score:2]
miR-212 also Regulates Cocaine Intake through Striatal MeCP2. [score:2]
miR-212 Regulates Cocaine Intake through Striatal CREB Signaling. [score:2]
Besides cancer, miR-212 has also been implicated in regulating organogenesis by playing a key role in modulating epithelial stromal interactions (Ucar et al., 2010). [score:2]
miR-212 and miR-132 are required for epithelial stromal interactions necessary for mouse mammary gland development. [score:2]
Two recent studies from our group have identified a key role for miR-212, also encoded by the miR-212/132 gene cluster, in regulating compulsive-like cocaine intake in rats (Hollander et al., 2010; Im et al., 2010). [score:2]
These findings identify miR-212 as a novel cocaine-responsive gene that is up regulated in the striatum in response to cocaine overconsumption that serves to promote CREB activity through positive feedback and thereby attenuate the motivational properties of the drug. [score:2]
Future studies in this respect could further help in improving our understanding of how miR-212 and miR-132 regulate different neuronal and non-neuronal functions or if these two miRNAs are functionally redundant? [score:2]
We therefore hypothesized that miR-212-MeCP2 interactions may regulate cocaine intake by influencing levels of BDNF in striatum. [score:2]
Regulation of the miR-212/132 locus by MSK1 and CREB in response to neurotrophins. [score:2]
The miR-212/132 Cluster. [score:1]
The first study showed that in rats with extended access to cocaine (6 h per day) there is a ∼1.75-fold increase in both striatal miR-212 and miR-132 levels (Hollander et al., 2010). [score:1]
Moreover, as miR-132 and miR-212 share the same seed region, this suggests that miR-212 may similarly repress MeCP2. [score:1]
The miR-132/miR-212 family of miRNAs was first identified in a genome wide search for genes responsive to the transcription factor cAMP response element binding protein (CREB) using an approach termed Serial Analysis of chromatin occupancy (SACO) (Impey et al., 2004). [score:1]
Taken together, these studies highlight the fact that miR-212 plays a critical role in fine-tuning transcriptional and neuroplastic responses to drugs of abuse. [score:1]
Specifically, we found that miR-212 can control cocaine intake through two complementary mechanisms: amplifying CREB signaling and reducing MeCP2/BDNF transmission in striatum. [score:1]
Dominant negative or phosphorylation -deficient mutant forms of CREB attenuated these stimulatory effects of miR-212 on CREB signaling. [score:1]
Cocaine Intake and miR-212. [score:1]
Analysis of the promoter for this miRNA gene cluster reveals the presence of multiple cAMP response element (CRE) sites and experimental evidence verifies that these miRNAs are indeed CREB inducible (Vo et al., 2005); (see Figure 1) Recent studies from Remenyi et al. have shown that this gene cluster in fact produces four mature miRNAs, namely miR-132, miR-132*, miR-212, and miR-212*, where miR-132* and miR-212* are encoded by the same primary transcript, but on the opposite strand, as the miR-132 and miR-212 miRNAs, respectively (Remenyi et al., 2010). [score:1]
Non-Neuronal Roles of miR-212. [score:1]
We found that miR-212 increases activity -dependent production of cAMP by sensitizing adenylyl cyclase activity. [score:1]
Consistent with a profound stimulatory effect of miR-212 on CREB in cultured cells in vitro, we found that levels of CREB that was phosphorylated at serine 133 (i. e., activated CREB) was significantly increased (Hollander et al., 2010). [score:1]
Hence, homeostatic interactions between miR-212 and MeCP2 may determine vulnerability to cocaine addiction. [score:1]
Shown are mouse/human miR-212 and miR-132 genes, with locations of CRE elements through which CREB can stimulate miR-212 and miR-132 transcription. [score:1]
These findings support the hypothesis that miR-212 controls cocaine intake at least in part by amplifying the CREB-TORC signaling axis in striatum. [score:1]
Besides playing a critical role in drug -induced neuroplasticity relevant to addiction, there is emerging evidence that miR-212 is also involved in a host of other biological and pathophysiological processes. [score:1]
Figure 1 The miR-212/132 gene cluster is located on chromosome 17 in humans, 10 in rats, and 11 in mouse. [score:1]
More importantly, we also found that miR-212 amplified CREB signaling in the striatum in vivo. [score:1]
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2
[+] score: 117
Other miRNAs from this paper: mmu-mir-132, mmu-mir-212, rno-mir-132
It has been reported that miR-212-3p promoted angiogenesis to attenuate ischemic heart disease by inhibiting the expression of Rasa1/Spred1, thus upregulating Ras/mitogen-activated protein kinase [17]. [score:10]
Zhao JL miR-212/132 downregulates SMAD2 expression to suppress the G1/S phase transition of the cell cycle and the epithelial to mesenchymal transition in cervical cancer cellsIUBMB Life. [score:8]
The qPCR and western blot results showed that the miR-212-3p mimic inhibited NR4A2 –expression (Fig.   7d, e), as well as the expression of p53 and Bax. [score:7]
org) predicted that miR-212-3p was a putative miRNA targeting NR4A2 based on target sequences at the NR4A2 3′ untranslated region (UTR). [score:7]
In our research, we found that miR-212-3p expression decreased in ischemia, and its target NR4A2 increased, inhibiting the apoptosis of cardiomyocytes. [score:7]
The graphic image shows that ischemia inhibited the expression of miR-212-3p, thus increasing its target NR4A2 levels. [score:7]
Data are expressed as the mean + S. D. * P < 0.05; ** P < 0.01; n = 3To verify the regulation of NR4A2 by miR-212-3p, we cloned the wild-type 3′UTR sequence of NR4A2 into a luciferase reporter vector (Fig.   7c), and then we performed a luciferase reporter assay to determine whether miR-212-3p could directly regulate the expression of NR4A2 in H9c2 cardiomyocytes (Fig.   8). [score:7]
Data are expressed as the mean + S. D. * P < 0.05; ** P < 0.01; n = 3 To verify the regulation of NR4A2 by miR-212-3p, we cloned the wild-type 3′UTR sequence of NR4A2 into a luciferase reporter vector (Fig.   7c), and then we performed a luciferase reporter assay to determine whether miR-212-3p could directly regulate the expression of NR4A2 in H9c2 cardiomyocytes (Fig.   8). [score:7]
An inhibitor of miR-212-3p suppressed the cleavage of PARP and caspase3, and thus it inhibited cardiomyocyte apoptosis as NR4A2 did, whereas a miR-212-3p mimic did not affect the above-mentioned apoptosis markers, perhaps because apoptosis was saturated (Fig.   7b). [score:7]
In this study, the preliminary miRNA microarray results associated with predictive analysis by TargetScan suggested that miR-212-3p was the potential miRNA targeting NR4A2. [score:5]
It was reported that miR-132, one member of the miR-132/212 cluster, is induced by H [2]O [2] to target NR4A2 to aggravate apoptosis [33], but whether NR4A2 is the target of miR-212-3p in cardiomyocytes was unknown. [score:5]
NR4A2 was the target of miR-212-3p. [score:3]
e H9c2 cells were transfected with miR-212-3p inhibitor or mimic in ischemic conditions, and then, NR4A2, p53 and Bax were detected by western blot. [score:3]
First, miR-212-3p expression and function was detected in cardiomyocytes exposed to ischemia. [score:3]
b H9c2 cells were transfected with inhibitor or mimic of miR-212-3p followed by serum deprivation for 12 h. Changes in PARP, caspase3 and LC3 were analyzed by western blot. [score:3]
NR4A2 was the target of miR-212-3p in cardiomyocytes. [score:3]
MiR-212-3p is the upstream regulator of NR4A2 expression in ischemic cardiomyocytes. [score:3]
Expression of miR-212-3p was analyzed by qPCR. [score:3]
d H9c2 cells were transfected with miR-212-3p inhibitor in ischemic conditions, and NR4A2 levels were detected by qPCR. [score:3]
Most research on miR-212-3p has focused on its roles in the development of tumors and neurons, but its function in heart has been less reported 15, 16. [score:2]
MiR-212-3p possesses highly conserved sequences among vertebrates, and its expression is high in both the brain and heart, suggesting that it has an important role in the heart. [score:2]
Remenyi J Regulation of the miR-212/132 locus by MSK1 and CREB in response to neurotrophinsBiochem. [score:2]
c Website-predicted target of miR-212-3p and luciferase reporter plasmid containing the native NR4A2 3’UTR was co -transfected with miR-212-3p mimic in HEK293 cells for 24 h followed by a dual-luciferase activity assay. [score:2]
All the data verified that miR-212-3p is the upstream regulator of NR4A2 (Fig.   7c–e). [score:2]
Then, luciferase reporter plasmids were co -transfected with control or miR-212-3p mimic into HEK293 cells with Lipofectamine 2000 (Invitrogen). [score:1]
Currently, the function of miR-212-3p in ischemia -induced cardiomyocyte apoptosis is unknown. [score:1]
Here, we studied the role of NR4A2 in ischemia -induced cardiomyocyte apoptosis and autophagy and reported a miR-212-3p/NR4A2/p53/Bax pathway in autophagy -dependent apoptosis in ischemia-stimulated cardiomyocytes. [score:1]
The qPCR showed that miR-212-3p decreased in ischemic conditions (Fig.   7a). [score:1]
MiR-212-3p has been shown to have important roles in regulating cardiac hypertrophy [32]. [score:1]
Furthermore, we reported a new role of miR-212-3p in cardiomyocyte apoptosis and autophagy. [score:1]
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3
[+] score: 101
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
ACTH up-regulated the expression of miRNA-212, miRNA-182, miRNA-183, miRNA-132, and miRNA-96 and down-regulated the levels of miRNA-466b, miRNA-214, miRNA-503, and miRNA-27a. [score:9]
Both ACTH and 17α-E2 up-regulated the expression of miRNA-212, miRNA-132, miRNA-154, miRNA-494, miRNA-872, miRNA-194, and miRNA-24-1, but reduced the expression of miRNA-322, miRNA-20b, miRNA-339, miRNA-27a, miRNA-551b, and miRNA-1224. [score:8]
Real-time quantitative PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats. [score:7]
Real-time PCR (qRT-PCR) measurements demonstrated that ACTH treatment upregulated the expression of miRNA-212, miRNA-183, miRNA-182, miRNA-132 and miRNA-96, while down -regulating the expression of miRNA-466b, miRNA-214, miRNA-503 and miRNA-27a. [score:7]
qRT-PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats (Fig. 3 ). [score:7]
The levels of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377, and miRNA-96 were up-regulated, whereas miR-125b, miRNA-200b, miR-122, miRNA-466b, miR-138, miRNA-214, miRNA-503 and miRNA27a were down-regulated in response to 17α-E2 treatment. [score:7]
Treatment of MLTC-1 cells with Bt [2]cAMP for 6 h increased the expression of miRNA-212, miRNA-183, miRNA-132, miRNA-182 and miRNA-96 and inhibited the expression of miRNA-138 and miRNA-19a (Fig. 4B ). [score:7]
Treatment of MLTC-1 cells with Bt [2]cAMP for 6 h increased the expression of miRNA-212, miRNA-183, miRNA-132, miRNA-182 and miRNA-96, and inhibited the expression of miRNA-138 and miRNA-19a. [score:7]
Bt [2]cAMP stimulation of granulosa cells caused down-regulation of a majority of miRNAs, including miRNA-200b, miRNA-466b, miRNA-27a, miRNA-214, miRNA-138 and miRNA-19a, but expression levels of miRNA-212, miRNA-183, miRNA-182, and miRNA-132 were significantly increased. [score:6]
The level of expression of miR-212 and miR-132 was up-regulated (>1.5-fold) by both ACTH and 17α-E2 treatments. [score:6]
qRT-PCR measurements indicated that exposure of primary rat granulosa cells to Bt [2]cAMP for 24 h inhibited the expression of miRNA-200b, miRNA-466b, miRNA-27a, miRNA-214, and miRNA-138 and miRNA-19a while enhancing the expression of miRNA-212, miRNA-183, miRNA-182, and miRNA-132 (Fig. 4 ). [score:5]
Real-time PCR (qRT-PCR) confirmed ACTH -mediated up-regulation of miRNA-212, miRNA-183, miRNA-182, miRNA-132 and miRNA-96. [score:4]
The precursor for miRNA-212 was also up-regulated. [score:4]
ACTH treatment caused maximum up-regulation of two miRNAs, miRNA-212 and miRNA-132, with a fold-stimulation of 4.23 and 3.43, respectively. [score:4]
We next evaluated the effects of Bt [2]cAMP stimulation of rat ovarian granulosa cells and of mouse MLTC-1 Leydig tumor cells on the expression of twelve miRNAs (miRNA-212, miRNA-122, miRNA-183, miRNA-200b, miRNA-466b, miRNA-182, miRNA-96, miRNA-27a, miRNA-132, miRNA-214, miRNA-138 and miRNA-19a) whose adrenal expression was differentially altered in response to treatment of rats with ACTH, 17α-E2 or DEX. [score:3]
The levels of expression of miRNA-212, miRNA-122, miRNA-138, miRNA-214, miRNA-183, miRNA-182, miRNA-132, miRNA-96, miRNA-466b, miRNA-200b, and miRNA-19a are shown. [score:3]
More specifically, we assessed the impact of Bt [2]cAMP treatment on the expression of miRNA-212, miRNA-122, miRNA-27a, miRNA-466b, miRNA-200b, miRNA-138, miRNA-214, miRNA-183, miRNA-182, miRNA-132, miRNA-96 and miRNA-19a. [score:3]
0078040.g003 Figure 3Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
Moreover, cultured mouse granulosa cells exhibited a robust induction of miRNA-132 and miRNA-212 when challenged with 8BrcAMP [36]. [score:1]
Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
One study reported a robust induction of miRNA-21, miRNA-132 and miRNA-212 following in vivo stimulation of mouse ovaries with LH/hCG [36]. [score:1]
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4
[+] score: 88
DARPP-32, which is phosphorylated by PKA, accumulates in the nucleus of striatal neurons and inhibits PP1, leading to increased histone H3 phosphorylation [44] The observed upregulation of miR-212 and miR-132 in the dorsal striatum following extinction training in rats with a history of cocaine SA may be associated with posttranslational modifications (PTMs) of histones that are induced by daily cocaine administration and the subsequent changes in dopamine and glutamate transmission (see Fig.   6). [score:8]
Our results demonstrate the upregulation of mature miR-132 and miR-212 expression in the rats following cocaine SA, but not after 14 days of intake in either the YC or YS groups. [score:6]
To assess whether cocaine induced long-lasting changes in the expression level of striatal miRNAs that are important for synaptic plasticity, we analyzed the expression pattern of miR-124, miR-132, miR-134, and miR-212 after 14 days of the SA of the drug and after the 10-day extinction training (Table 2). [score:5]
Finally, miR-212/132 cluster, composed of two miRNAs sharing close sequences, was identified as a target of CREB and REST protein that control its own expression [16]. [score:5]
Possible explanations for the miR-212 and miR-132 upregulation during the self-administration phase and its persistence during extinction training may include multiple cocaine -induced mechanisms, such as changes in dopamine and glutamate neurotransmission, alterations in specific signaling pathways, and/or epigenetic regulation. [score:5]
The hypothesis that miR-212 may regulate its own (long-lasting) expression during cocaine SA by enhancing the activity of the CREB/TORC signaling cascade seems promising; however, it needs to be tested. [score:4]
We postulate that the long-term upregulation of the miR-212/132 and REST mRNA levels is due to chromatin remo deling; however, additional studies, including chromatin immunoprecipitations, should be performed to determine the changes in histone modifications close to these loci. [score:4]
These proteins are important for controlling dendritic spine morphology and synaptic plasticity, and they regulate the expression, processing, and function of many miRNAs, such as miR-212/132 (Fig.   7). [score:4]
Consistent with the above cited findings, it is very likely that the long-term upregulation of miR-212 and miR-132 is governed by epigenetic mechanisms. [score:4]
Furthermore, the post hoc test indicated that the levels of miR-212 and miR-132 were only significantly upregulated in the rats with a cocaine SA history (1.5-fold, p < 0.01 and 1.7-fold p < 0.001, respectively) (Fig.   3b). [score:4]
Consistent with the above findings, in this study, we analyzed the expression of miR-124, miR-132, miR-134, and miR-212, as well as the levels of the Ago2, Pum2, and REST mRNAs and proteins following cocaine self-administration (SA) and its withdrawal with using extinction training (neither cocaine delivery nor the presentation of the conditioned stimulus) in rats. [score:3]
A recent study has elegantly demonstrated that miR-212 is highly responsive to increased expression of CREB and its essential coactivators TORCs and Ser-133 phosphorylation in the dorsal striatum 24 h after the last cocaine self-administration session in rats with extended access to the drug [19]. [score:3]
For the first time, our data showed that cocaine SA and extinction training is able to significantly increase the expression levels of the mature miR-212 and miR-132 transcripts in rats. [score:3]
The later finding extends the recent observations of Hollander et al. who demonstrated that 6-h (but not 1 h) access to cocaine SA for 7 days increased miR-132 and miR-212 expression in the rat striatum [19]. [score:3]
This mechanism may be involved in the expression of either miR-212/132 cluster or miR-132 alone. [score:3]
Additionally, there were significant differences in the expression patterns of miR-212 (p < 0.01) and miR-132 (p < 0.001) between the cocaine SA-2 and YC-2 groups (Fig.   3b). [score:3]
Fig. 6The putative signaling pathways involved in long-term miR-212/132 expression. [score:3]
Similarly, the level of miR-212 is relatively high in the rat striatum [21], where extended access to cocaine self-administration increases its expression level. [score:3]
Furthermore, miR-212 may amplify CREB activity through positive feedback signaling; miR-212 activates Raf1 (the kinase that phosphorylates and sensitizes adenylyl cyclase), at least in part, via SPRED1 repression (a Raf1 suppressor) [19]. [score:3]
Fig. 3The expression pattern of miR-212 and miR-132 in the rat striatum after cocaine self-administration (a) and 10-day extinction training (b). [score:3]
Interestingly, four different CRE sites and one REST site are present within the regulatory region of the miR-212/132 cluster (Fig.   6). [score:2]
Importantly, it was established that knockdown of miR-212 enhances cocaine rewarding properties in self-administration procedures [19]. [score:2]
miRNAs with FC ≥1.3 and p < 0.05 were considered to be differentially expressed (indicated in bold) compared to the YS group SA self-administered group, YC yoked cocaine group, YS yoked saline (control) group We observed that the 14th day of cocaine SA had a significant effect on the level of miR-212 (F [(2, 15)] = 7.41, p < 0.01) and miR-132 (F [(2, 15)] = 5.50, p < 0.05). [score:1]
miRNAs with FC ≥1.3 and p < 0.05 were considered to be differentially expressed (indicated in bold) compared to the YS group SA self-administered group, YC yoked cocaine group, YS yoked saline (control) group We observed that the 14th day of cocaine SA had a significant effect on the level of miR-212 (F [(2, 15)] = 7.41, p < 0.01) and miR-132 (F [(2, 15)] = 5.50, p < 0.05). [score:1]
Surprisingly, the significant increase in the miR-132 and miR-212 levels was long-lasting and remained in the rats that had been withdrawn from cocaine SA. [score:1]
Moreover, a statistically significant difference (p < 0.01) was observed in the level of miR-212 between the cocaine SA-1 and YC-1 groups (Fig.   2a). [score:1]
Recently, it was demonstrated that four miRNAs (miR-124, miR-132, miR-134, and miR-212) are especially important for neuronal function, plasticity, and/or substance use disorder. [score:1]
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5
[+] score: 79
Other miRNAs from this paper: rno-mir-132, rno-mir-137
Our results show miR-132 and miR-212 are increased 50% on day 1 and 2–2.5 fold on day 7 (Fig 1C), in contradiction to the notion that reduced expression of these miRNAs causes MeCP2 translational upregulation. [score:8]
These oligonucleotides effectively suppressed the expression of respective miRNA (Fig 1E) but had no significant effects on MeCP2 protein levels (Fig 1F), suggesting that miR-132 and miR-212 do not regulate MeCP2 expression. [score:8]
As seen in HSC with canonical Wnt pathway inhibition, the pan-NADPH oxidase (NOX) inhibitor diphenyleneiodonium (DPI) reduces MeCP2 and non-phospho-β-catenin proteins and restores Ppar-γ expression and HSC quiescence but without changes in miR132 and miR212. [score:7]
The present study examined the roles of miR132 and miR212 which share sequence homology and targets [15] in MeCP2 expression and MeCP2 -mediated Ppar-γ regulation in Wnt- and NOX -mediated activation of HSCs. [score:6]
NOX inhibition with DPI reduces MeCP2 and non-phosphorylated β-catenin, upregulates Ppar-γ, and inactivates HSC without changing miR-132 and miR-212. [score:6]
miR-132 and miR212 are upregulated during culture activation of rat primary HSC. [score:4]
Wnt antagonism with FJ9 reduces MeCP2 protein and upregulates Ppar-γ in a manner independent of miR-132 and miR-212. [score:4]
To assess the causal link between induced miR-132/miR212 and MeCP2 -mediated Ppar-γ upregulation, we transfected anti-miR-132 and anti-miR-212 oigos in FJ9 -treated HSC. [score:4]
Using our TaqMan method with 4.5S RNA as the house keeping RNA, the levels of miR-132 and miR-212 are shown not to be reciprocal to MeCP2 protein expression in HSC in vitro and in vivo mo dels. [score:3]
We then transfected anti-miR-132 or/and anti-miR212 oligonucleotides (oligos) into cultured aHSC to determine their effects on MeCP2 protein expression. [score:3]
To examine this inductive effect on miR-132/miR-212 at transcriptional level, we tested the HSC line BSC transfected with the plasmid which expresses luciferase downstream of four deletion fragments of the promoter and the region between the two miRNA sequences as depicted in Fig 2F. [score:3]
0156111.g005 Fig 5 miR-132 and miR-212 are highly conserved among vertebrates and share similar sequences, thus are predicted to have common targets [15]. [score:3]
To further examine this intriguing mechanism and potential contribution of miR-212, we quantified by TaqMan qPCR, the levels of mature miR-132 and miR212 in parallel with assessment of MeCP2 mRNA and protein expression in rat primary HSC from day 0 to day 7 of culture on plastic. [score:3]
miR-132 and miR-212 levels are not reciprocal with MeCP2 protein expression in activation of HSC. [score:3]
miR-132 and miR-212 are highly conserved among vertebrates and share similar sequences, thus are predicted to have common targets [15]. [score:3]
In summary, our results do not support the roles of miR-132 and miR-212 in regulating MeCP2 protein in HSC activation in culture or in vivo. [score:2]
To assess transcriptional regulation for the miR-212 and miR-132 cluster, promoter deletion-luciferase constructs (-1205/-74, -725/-75, -468/+293, +29/+293) were generated by cloning different lengths of the promoter and regions between the two miRNA sequences into the pGL3-basic vector (Promega) as described [17]. [score:2]
To test knockdown effects of miR-132 and miR-212, anti-oligonucleotides for these miRNAs (Invitrogen) were introduced into cultured rat HSC by electroporation using the Neon [TM] Transfection System (Invitrogen). [score:2]
In contrary to previous report, our results failed to validate the roles of miR132 or miR212 in MeCP2 regulation in HSC. [score:2]
However, the levels of neither miR-132 nor miR-212 are changed by DPI (Fig 3D), suggesting the observed effect on MeCP2 is independent of these miRNAs. [score:1]
FJ9 treatment increases both miR-132 and miR-212 (Fig 2E). [score:1]
Anti-oligonucleotides effectively abrogate miR-132 and miR-212 but do not reduce MeCP2 protein in aHSC. [score:1]
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6
[+] score: 49
0018613.g004 Figure 4Three general trends of miRNA expression trajectories were observed for Wistar islets at 2.8G vs 16.7G: i) increased expression as exhibited by rno-miR-132, rno-miR-212 and rno-miR-409-3p, ii) decreased expression as in the case of rno-miR-124, rno-miR-142-3p, rno-miR-375, rno-miR-335, rno-miR-130a and rno-miR-708 and, iii) no change as seen in rno-miR-376a, rno-miR-142-5p and rno-miR-433. [score:7]
Three general trends of miRNA expression trajectories were observed for Wistar islets at 2.8G vs 16.7G: i) increased expression as exhibited by rno-miR-132, rno-miR-212 and rno-miR-409-3p, ii) decreased expression as in the case of rno-miR-124, rno-miR-142-3p, rno-miR-375, rno-miR-335, rno-miR-130a and rno-miR-708 and, iii) no change as seen in rno-miR-376a, rno-miR-142-5p and rno-miR-433. [score:7]
The deregulated expression of mir-132 and mir-212 in different experimental mo dels strongly links these miRNAs to common pathways underlying the disease pathologies of diabetic GK rats and obese mouse mo dels. [score:6]
Using assays [24] we validated the expression of ten most upregulated miRNAs from the significant list, and also prioritizing miRNAs which appeared in previous studies on pancreatic islets or insulin-secreting beta cell lines such as miR-124, miR-376a, miR-132 and miR-212. [score:5]
Interestingly, miR-212 and miR-132 have also been shown to be upregulated in isolated pancreatic islets in the obese phenotypes of both the diabetes-resistant (B6) and diabetes-susceptible (BTBR) mouse mo dels [32]. [score:4]
Four of the glucose-regulated miRNAs found in this study, mir-124, mir-212, mir-132, and mir-409-3p, were previously reported to be upregulated in the mouse insulin secreting cell line, MIN6, after 16 h stimulation in 25 mM glucose [31], which is noteworthy despite that tumour-derived cell lines have been shown to generally exhibit significantly different miRNA signature compared to primary cells [6]. [score:4]
We specifically found expression of rno-miR-130a, rno-miR-132, rno-miR-212 and rno-miR-335 to be regulated by hyperglycaemia. [score:4]
We saw changes in miRNA expression manifested within a short temporal window of only one hour, such as for rno-miR-130a, rno-miR-132, rno-miR-212 and rno-miR-335. [score:3]
This is clearly seen for rno-miR-212, rno-miR-132, and rno-miR-130a, whose expression levels in the GK and Wistar islets eventually coincide at 16.7G (Fig. 4). [score:3]
In general, aside from more significant changes in expression levels of miRNAs at 24 h incubation compared to 1 h incubation, three trends in terms of expression changes are also observed in the Wistar islet upon stimulation at 16.7G as compared to 2.8G: i) increasing miRNA levels, as displayed by rno-miR-132, rno-miR-212 and rno-miR-409-3p, ii) decreasing miRNA levels as exhibited by rno-miR-124, rno-miR-142-3p, rno-miR-375, rno-miR-335, rno-miR-130a and rno-miR-708, and iii) no significant change as displayed by rno-miR-376a, rno-miR-142-5p and rno-miR-433. [score:3]
In contrast, rno-miR-212 and rno-miR-132 showed the opposite trend leading to decreased miRNA levels upon stimulation at 16.7 G. Thus, for miRNAs that increases with increasing glucose concentrations in the normal Wistar islets, the GK islet miRNAs levels go down (rno-miR-132 and rno-miR-212) or do not change (rno-miR-409-3p), whereas for miRNAs whose levels decrease with increasing glucose concentration in Wistar islets, the GK islet miRNAs is also reduced (e. g. rno-miR-124, rno-miR-142-3p, rno-miR-375) (Fig. 4). [score:1]
This trend was particularly distinct for both miR-212 and miR-132, which belong to the same gene cluster being only 200 nt apart and containing identical seed sequences. [score:1]
Among the miRNAs tested only rno-miR-130a, rno-miR-132, rno-miR-212 and rno-miR-335 responded to glucose stimulation at either 8.3 mM or 16.7 mM in the healthy Wistar islets (Fig. 3; p<0.05). [score:1]
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7
[+] score: 47
Collectively, chronic alcohol consumption superimposed on overnutrition -mediated cardiac pathology can putatively induce the following signaling mechanisms: (1) inhibition of mTORC1 and attenuation of protective compensatory mechanisms; (2) inhibition of INS metabolic signaling via downregulation of INS receptor, IRS-1, GLUT4; (3) downregulation of growth inhibitory mir-200 family microRNAs and (4) upregulation of mir-212 (Figure 4). [score:16]
Since alcohol is shown to up-regulate mir-212 in other cell types, it is conceivable that alcohol -mediated upregulation of mir-212 can be one of the mechanisms by which alcohol exacerbates cardiomyopathy. [score:7]
Alcohol -mediated upregulation of the micoRNA mir-212 is implicated in alcoholic liver disease [115]. [score:6]
In such conditions, upregulation of mir-212 by both alcohol and Ang II can lead to activation of fetal gene program and heart failure. [score:4]
Mir-212 has been shown to be upregulated by ethanol in intestinal cells [115] and Ang II in cardiac fibroblasts, which is associated with activation of ERK1/2 pathway [125]. [score:3]
Thus mir-212 can be a potential therapeutic target to protect the heart in conditions of overnutrition and chronic alcoholism. [score:3]
The mir-212 is overexpressed in failing hearts. [score:3]
The significance of CREB phosphorylation emerges from a study reporting regulation of mir-212 in a CREB -dependent manner involving ERK1/2 activation [127]. [score:2]
In this regard, the role of mir-212 is noteworthy. [score:1]
Interestingly, mir-212 has emerged as an activator of fetal gene program [116, 117]. [score:1]
Additionally, transfection of isolated adult rat cardiomyocytes with a set of fetal miRNAs (miR-21, miR-129, and miR-212) induced cellular hypertrophy and activation of a fetal gene program [117]. [score:1]
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8
[+] score: 39
These were both targeted by miR-137, which appeared to have the greatest overall effect, whereas miR-212 had the least effect on these target gene constructs. [score:5]
Prominent among this group were miRNAs that are enriched in neurons and associated with developmental regulation (let-7i, let-7f, let-7b, miR-98), cell cycle regulation (miR-137, mIR-128) and neural activity (miR-132, miR-212). [score:4]
Similarly, the results suggest a role for miR-212 in brain development with expression levels increased more than four-fold in the telencephalon between E12 and birth. [score:4]
MiR-212 and miR-132 are tandem miRNAs with similar target specificity due to their identical seed sequences. [score:3]
Enriched ontologies of putative target genes of miR-98, miR-212 and miR-137 were identified using the DAVID online database. [score:3]
Microarray expression data was validated by RT-PCR for miR-98 (B), miR-212 (E) and miR-137 (H) with correlation coefficients of 0.64 (C), 0.62 (F) and 0.69 (I) respectively. [score:3]
In particular, regulation of 3’-UTR elements from Wnt7a (miR-137) and Gpr88 (miR-137) was particularly strong and, along with Clasp2 (miR-98) and Rab15 (miR-212) provides support for the role of post-transcriptional regulation in axon and dendritic growth, maturation and function [35– 38]. [score:3]
Consistent with the increase of miR-212 expression between E12 and E19, Cbll1 function is demonstrated to be most vital in the early stages of embryogenesis, with its contribution declining in later stages [49]. [score:3]
To generate reporter vectors bearing binding sites for the three miRNA examined in detail, miR-98, miR-212 and miR-137, oligonucleotides encoding target gene miRNA recognition elements (MREs) were annealed to form SpeI and HindIII restricted overhangs of a ligatable cassette compatible with SpeI and HindIII digested pMIR-REPORT vector (Ambion, Austin, TX) as described previously [69, 70]. [score:3]
Figures show the normalised signal intensity values for miR-98 (A) and miR-212 (D) and miR-137 (G) at each developmental stage in the mesencephalon and telencephalon (*** = p < 0.001). [score:2]
Our luciferase reporter assays support miR-212 involvement in neurodevelopment via regulation of Rab15, member RAS oncogene family (Rab15) and Cbl proto-oncogene-like 1, E3 ubiquitin protein ligase (Cbll1). [score:2]
Dysregulation of miR-212 is associated with drug addiction [44], neuropathological disorders [43] and schizophrenia [45]. [score:2]
MiR-212 arises from the miR-212/132 cluster, which is highly conserved in vertebrates. [score:1]
In the brain, miR-212 and miR-132 play vital roles in the formation and plasticity of neuronal connections, and long-term synapse activation (reviewed [42, 43]). [score:1]
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9
[+] score: 35
ARB treated patients (n = 16) revealed a significant attenuation of miR-132 expression (0.55-fold), as well as a tendency for miR-212 downregulation (0.64-fold), as compared to non-ARB -treated patients (miR-132; 0.93 and miR-212; 1.01) (n = 16) (Figure 5B). [score:5]
Despite these limitations, we observed a significant downregulation of miR-132, as well as a robust attenuation of miR-212 in the ARB -treated patients. [score:4]
Interestingly, even though the ET-1 -induced hypertension had a much shorter duration than the sustained hypertension induced by AngII, both miR-132 and miR-212 were upregulated at a point in time when blood pressure was not (Figure 4). [score:4]
Furthermore, miR-132 was found to be significantly upregulated in the plasma of AngII -induced hypertensive animals, whereas no regulation was observed for plasma miR-212 levels compared to the control rats (Figure 2B). [score:4]
Even though miR-132 and miR-212 are expressed from the same precursor, we observed independent regulation in the different tissues in response to the same AngII infusion. [score:4]
For example, miR-132 and miR-212 are clustered closely in the genome and are transcribed together under the regulation of cAMP response element binding protein [8], which is a known AngII regulated gene [9, 10]. [score:3]
Lack of miR-212 upregulation in the plasma of AngII -induced hypertensive rats compared to control rats might be caused by the low concentration and high variability of the miR-212 levels found in the plasma. [score:3]
Since the miR-132 gene is clustered with the miR-212 gene and they are likely expressed together [21], we included miR-212 in further analyses. [score:3]
Since no anti-miR experiments have been conducted, it has not been possible to deduce the specific cause and effect relationship; however, the regulation of miR-132 and miR-212 is likely biological important, because although rats and humans share biological features in blood pressure control, they have multiple differences in the molecular subtypes of ion channels, receptors and signaling pathways in blood vessel cells. [score:2]
Further studies are necessary to assess the relative biological and pharmacological impact of individual miR-132 and miR-212 levels on systemic blood pressure, in the heart, arterial wall and kidney. [score:1]
Thus, AT [1]R activation in rats increases miR-132 and miR-212, while blocking the AT [1]R decreases miRNA levels in humans. [score:1]
Our results suggest that miR-132 and miR-212 are involved in AngII -induced Gαq-signaling pathway leading to hypertension. [score:1]
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10
[+] score: 27
Other miRNAs from this paper: rno-mir-132
In the present study we disclosed that the gene designated prt6, encoding non-coding RNAs with the sequences of EST 1392108_at (Affymetrix), miR-212, and miR-132, is development- and PCP-regulated gene in the rat thalamus, and that the schizophrenomimetic NMDA receptor antagonist elicits a significant increase in the expression levels of prt6 at PD32 and 50, but not PD8, 13, 20 and 25. prt6 RNAs are strongly expressed in the brain and testis, and are also upregulated by PCP in the neocortex and hippocampus of young adult rats at PD50. [score:10]
In agreement with this, our recent DNA microarray experiments showed that PCP administered with the same regimen as in the present study suppresses the neocortical expression of the predicted targets of these two miRNAs, PAIP2A and H2AFZ (unpublished data), suggested by sequence analyses (miRanda and TargetScan) of miR-132 and miR212. [score:9]
The upregulated 3.0-kb (Fragment Y) product could act in the brain, at least in part, as a long primary transcript (pri-miRNA) for miR-132 and/or miR212, because the sequences of these micro -RNAs are tandemly located within the transcript. [score:4]
In terms of the NMDA receptor function-related and development -dependent schizophrenomimetic-responsive nature of prt6, it should be noted that miR-132 and miR-212, the sequences of which are found in prt6 RNA (Figure 2 ), have been reported to be dysregulated in the prefrontal cortex of postmortem brains from schizophrenic patients [43]– [45]. [score:3]
Instead, we speculated presence of a tandem array of microRNAs (miRNAs), miR-212 and miR-132, located upstream of the 5′ end of Fragment X (Figure 2A ). [score:1]
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[+] score: 24
These selected miRNAs included the seven most strongly upregulated miRNAs (miR-330, miR-338, miR-223, miR-20a, miR-181a, miR-592, miR-212) in the Ago2 IP at 30 min, the only downregulated miRNA (miR-29b) in the Ago2 IP at 30 min, and the three most strongly upregulated miRNAs (miR-219, miR-384, let-7f) in the Ago2 IP at 120 min post-HFS (significant by t-test with Dunn–Bonferroni correction and 1-Way ANOVA with LSD test). [score:10]
When comparing miRNA Ago2/input expression ratios, eight miRNAs (miR-384, miR-29b, miR-219, miR-592, miR-20a, miR-330 miR-223, and miR-34a) exhibited increases relative to the contralateral dentate gyrus, whereas five miRNAs (miR-let7f, miR-338, miR-212, miR-19a, and miR-326) showed decreases in this ratio. [score:3]
Target gene list sizes for miRNAs with activity -dependent association with Ago2 for the 8 enhanced miRNAs were 97 (miR-20a), 156 (miR-219), 58 (miR-223), 114 (miR-29b), 30 (miR-330), 91 (miR-34a), 156 (miR-384), and 53 (miR-592) and for the 5 depleted miRNAs were 52 (let-7f), 55 (miR-338), 47 (miR-212), 255 (miR-19a), 32 (miR-326). [score:3]
Consistent with our previous work (Wibrand et al., 2010), expression of miR-212 and miR-132 was increased in dentate gyrus lysates at 120 min post-HFS. [score:3]
In contrast, 3 miRNAs (miR-let7f, miR-338, and miR-212) exhibited decreased expression in the Ago2 IP relative to input. [score:3]
Wibrand and colleagues observed NMDAR -dependent decreases in mature miR-212 and miR-132 in the absence of NMDAR -dependent effects on precursor miRNA levels, suggesting that NMDAR signaling promotes decay of the mature miRNAs. [score:1]
Finally, miR-212 was elevated in the input sample, but was significantly decreased in abundance in the Ago2 pellet. [score:1]
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[+] score: 24
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Finally, other subsets of miRNAs were either up-regulated (miR-23a-3p, miR132-3p, miR-146a-5p, miR-154-3p, miR-181d-5p, miR-212-3p, miR-212-5p, miR-344b-5p, miR-380-3p, miR-410-3p, miR-433-3p and miR-3584; Fig. 2, Supplementary Fig. S4), or down-regulated (miR-29c-5p, miR-30a-5p, miR-30c-2-3p, miR-30e-3p, miR-138-5p, miR-140-3p, miR-551b-3p and miR-652-3p; Fig. 2, Supplementary Fig. S5) during all phases of the disease. [score:9]
Moreover, we and Gorter et al. 24 observed the up-regulation of miR-212-5p, whereas we and Bot et al. 23 observed the up-regulation of miR-433-3p. [score:7]
Cluster 1, composed by miR-674-3p, miR-505-3p and miR-212-5p, was up-regulated during epileptogenesis (4 and 8 days after SE). [score:4]
In fact, the expression patterns of miR-20b-5p, miR-142-3p, miR-181d-5p, miR-212-5p, miR-344b-5p and miR-674-3p were identical to those observed using the microarray, and those of miR-21-5p and miR-146a-5p were very similar, although not identical (Fig. 4). [score:3]
Cluster 4, together with cluster 1 (that includes miR-674-3p, miR-505-3p and miR-212-5p) and cluster 5 (including miR-144b-5p and miR-20b-5p), may also strongly influence neuronal activity. [score:1]
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[+] score: 21
Strikingly, two of the downstream targets of IGF-1 signalling, namely connexin 43 and zona occludens 1, are also validated targets for miR-206 [46], [55] and miR-212 [56], [57] (depleted from the cerebellum) respectively. [score:5]
Our data provides a detailed map of miRNA brain expression in rats and shows that there are some differences in the expression in the cerebellum of a subset of the detectable transcripts, which are either highly enriched (miR-206 and miR-497) or nearly depleted (miR-132, miR-212, miR-221 and miR-222). [score:5]
Biochim Biophys Acta 56 Tang Y Banan A Forsyth CB Fields JZ Lau CK 2008 Effect of alcohol on miR-212 expression in intestinal epithelial cells and its potential role in alcoholic liver disease. [score:5]
Forebrain enrichment was also seen for the two members of the miR-132 family (miR-132 and miR-212), which were also most highly expressed in the hippocampus and amygdaloid regions. [score:3]
Notably, we found reciprocal expression profiles for a subset of the miRNAs predominantly found (> ten times) in either the cerebellum (miR-206 and miR-497) or the forebrain regions (miR-132, miR-212, miR-221 and miR-222). [score:3]
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[+] score: 16
In a study on alcoholic liver disease in which alcohol -induced gut leakiness is a key factor, ethanol increased miR-212 expression, decreased the level of Zonula occludens 1 protein, disrupted tight junctions, and increased the permeability of monolayers of Caco-2 cells [34]. [score:5]
Hypoxia alone did not significantly affect miR-212 expression until the 10-day time point. [score:3]
Relative miRNA expression levels of miR-347 and miR-212 in the kidney following either 1, 5, or 10 days of hypoxia as determined by quantitative RT-PCR. [score:3]
The notion that DOR action could mimic the hypoxic change in miR-212 provides additional evidence since DOR activation is protective against hypoxic injury [6]– [8], [16]. [score:1]
Therefore, the hypoxic reduction of miR-212 may be an adaptive strategy of the kidney in response to hypoxia. [score:1]
This study suggests an adverse effect of increased miR-212 on tissues in pathophysiological conditions. [score:1]
With this chronic hypoxia, miR-212 levels were repressed to less than 40% of the control in all combinations of hypoxia and UFP-512 treatment tested (Figure 6b). [score:1]
In 5-day samples, miR-212 was largely reduced by UFP-512 in both the control and hypoxic conditions. [score:1]
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A) Expression level of miR-181a precursor, miR-181a-2, on the mRNA Exon array, B) expression level of mature miR-181a transcript on the miRNA array, C) expression level of mature miR-212 transcript miR-212 on the miRNA array. [score:7]
We observed a trend towards downregulation of miR-212 in the VTA on methamphetamine self-administration (Additional file 5: Figure S4). [score:4]
Boxplots showing expression levels of miR-181a and miR-212 on the arrays. [score:3]
In the dorsal striatum, miR-212 influences cocaine addiction behaviors [43]. [score:1]
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There are also a number of miRNAs such as miR-132, miR-212, miR-130a and miR-152 shown to be upregulated in the pancreatic islets of the wi dely-studied T2D mo del Goto-Kakizaki rats (Esguerra et al., 2011) with active roles in beta cell stimulus-secretion coupling (Malm et al., 2016; Ofori et al., 2017). [score:4]
miR-132 and miR-212 expression in INS-1 832/13 cells (A–B) or in EndoC-βH1 cells (C–D) at different confluences. [score:3]
Among the other miRNAs included in this study, we observed significantly higher expression levels of miR-132 and miR-212 at higher confluences in INS-1 832/13 cells (Figs. 3A– 3B) but only an increasing trend in the human EndoC-βH1 cells (Figs. 3C– 3D). [score:3]
The following primers from TaqMan [®] Gene Expression and TaqMan [®] miRNA Assays were used for qPCR: Cav1/CAV1 (Rn00755834_m1/Hs00971716_m1), Aifm1/AIFM1 (Rn00442540_m1/ Hs00377585_m1), miR-375 (TM_ 000564), miR-200a (TM_000502), miR-130a (TM_00454), miR-152 (TM_000475), miR-132 (TM_000457) and miR-212 (TM_002551) were used for qPCR. [score:1]
We also investigated the influence of confluence on the expression levels of miR-200a, miR-130a, miR-152, miR-132 and miR-212. [score:1]
Although we showed that miR-375, which is one of the most enriched beta cell miRNA was not significantly influenced by confluence level in cultured rat and human beta cell lines, we clearly demonstrated that miR-132 and miR-212 are more dependent on cellular densities, as was shown for some miRNAs in other cells types (Hwang, Wentzel & Men dell, 2009; Van Rooij, 2011). [score:1]
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In contrast, we found a more succinct, transient down-regulation of miR-132-3p, with a concurrent rapid and transient increase in the levels of the miR-132/212 primary transcript, but no alteration in the co-transcribed mature miR-212-3p. [score:4]
Together these data show a striking discrepancy in the LTP regulation of the primary and mature transcripts of miR-132-3p and miR-212-3p, suggesting that the LTP -induced reduction in mature miR-132-3p levels was also regulated by post-transcriptional mechanisms. [score:3]
Regulation of the miR-212/132 locus by MSK1 and CREB in response to neurotrophins. [score:2]
It is of note that we found no significant regulation at any time point of miR-212-3p, which is derived from the same primary transcript as miR-132-3p (20 min: p = 0.93; 5 h: p = 0.63; 24 h: p = 0.47; n = 4–5). [score:2]
Interestingly, previous studies have linked miR-132-3p and Mapk1, as levels of the pri-miR-132-3p/miR-212 cluster have been reported to be dependent on the Mapk pathway (Kawashima et al., 2010; Remenyi et al., 2010). [score:1]
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The most upregulated microRNAs were miR-132-3p, miR-212-3p and miR-21-5p, which were increased by 1.75, 1.83 and 1.89-fold respectively. [score:4]
The highest positive correlation of expression was observed for miR-132-5p and miR-212-5p (0.98) miR-132-3p and miR-212-3p (0.97), miR-708-5p and miR-374-5p (0.94), and miR-374-5p and miR-31a-5p (0.94). [score:3]
The largest increases in expression occurred in miR-212-3p, miR-132-3p and miR-21-5p at 1.54, 1.52 and 1.41 fold of the control levels respectively (Table 1). [score:3]
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In the normoxic cortex, UFP-512 induced a significant upregulation in miR-351 expression by over 65%, (Figure 4c), but did increase miR-20b-5p (Figure 4a) and miR-212 (Figure 4b) expressions. [score:8]
These same conditions depressed miR-212 levels by 3-fold (Figure 4b) and miR-351 by 5-fold (Figure 4c). [score:1]
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For example, Tang et al (6) reported that alcohol -induced overexpression of miR-212 resulted in gut leakiness by downregulation of a major component of tight junctions, Zonula occludens 1. Gut leakiness is a key factor in alcoholic liver disease. [score:8]
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Overexpression of miRNA-132 or miRNA-212 increased glucose-stimulated insulin secretion [17]. [score:3]
The inductions of miR-132 and miR-212 by GLP-1 were correlated with cyclic adenosine monophosphate (cAMP) production and were blocked by a protein kinase A inhibitor[17]. [score:3]
There were seven miRNAs reduced by over 50% (miR-380-5p, miR-139-5p, miR-743b-5p, miR-212-3p, miR-132-5p, miR-3592, and miR-201-5p) after liraglutide treatment. [score:1]
Recent studies reported that the signaling pathways triggered by GLP-1 in rodent and human pancreatic β-cells were complex, with miRNA-132 and miR-212 as two of the many miRNAs involved in GLP-1 activity. [score:1]
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In the mo del group, 17 miRNAs were downregulated, including miR-1, miR-133, miR-29, miR-126, miR-212, miR-499, miR-322, miR-378, and miR-30 family members, whereas the other 18 miRNAs were upregulated, including miR-21, miR-195, miR-155, miR-320, miR-125, miR-199, miR-214, miR-324, and miR-140 family members. [score:7]
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D. Effect of miR-204, miR-93, miR-17, miR-302d, miR-455, miR-212 or miR-30a overexpression on Nurr1 3’ UTR long. [score:3]
Seven miRNAs were selected: miR-17, miR-204, miR-455, miR-30a, miR-212, miR-302d and miR-93. [score:1]
The intersection of these 3 databases gave 14 miRNAs in common and we choose miR-204, miR-30a, miR-302d, miR-212, miR-93, miR-17 and miR-455 for further experimentation. [score:1]
The seed sites of miRNAs selected for the specific part of the long 3’UTR are: miR-204 in nucleotide 870, miR-212 in nucleotide 1014, miR-93 and miR-302d in nucleotide 1063, miR-17 in nucleotide 1070, miR-455 in nucleotide 1177 and miR-30a in nucleotide 1279. [score:1]
The precursor sequences of the miR-145, miR-302d, miR-130a, miR-204, miR-93, miR-17, miR-455, miR-212 and miR-30a were cloned on pEGP-CE vector, acquired from Cell Biolabs Inc (7758 Arjons Drive San Diego, CA 92126 USA). [score:1]
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Knockdown or over -expression of miR-212 levels in striatum is able to change cocaine intake behavior [9, 10]. [score:4]
miR-212 in striatum is reported to decrease responsiveness to the motivational properties of cocaine by activating CREB signaling. [score:1]
MiR-212 in the striatum is able to regulate cocaine self-administrated intake behaviors [9, 10]. [score:1]
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We found that miR-142, miR-200c, miR-212, miR-325, miR-361, miR-376c, miR-429, and miR-494 overexpression could down-regulate the CRH mRNA level (p < 0.05; Figure 6A), and there was no difference between these miRNAs and the negative miRNA control (p > 0.05) in terms of cell viability (Supplementary Figure S2A). [score:6]
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Moreover, miR-212 and miR-132 [45] were able to regulate autophagy in cardiomyocytes via their commonly targeting gene of Foxo3 expression. [score:6]
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Other miRNAs from this paper: rno-mir-132
Furthermore, they showed that cocaine stimulation of MeCP2 decreased the expression of miR-212 and miR-132 resulting in an increase of BDNF expression with an increase in cocaine intake. [score:5]
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Serum was also analyzed by Q-RT-PCR for a panel of 20 tissue enriched and potential miRNA biomarkers, including those identified for liver (cfa-miR-122 and -885), heart/muscle (cfa-miR-1, -133, and -206), testis (miR-34b/c), pancreas (cfa-miR-216), brain (cfa-miR-212), and ubiquitously expressed cfa-miR-193b. [score:3]
A total of 22 miRNAs (Additional file 6: Figure S5) were selected for qPCR validation including the following 14 biomarker candidates of organ toxicity: liver (cfa-miR-122 and -885), pancreas (cfa-miR-216a/b); heart (cfa-miR-499); muscle (cfa-miR-206); heart/muscle (cfa-miR-1, -133a/b, and -208); testis (cfa-miR-34b/c); and brain and sciatic nervous tissues (cfa-miR-212, -432, and -885), and 5 miRNAs reported in the literature (cfa-miR-21, -192, -193a/b, and -200). [score:1]
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Our data also established the up-regulation of all members of the let-7 and miR-7 gene families, as well as that of the four miRNAs encoded by the miR-132/212 cluster, i. e. miR-132-3p, miR-132-5p, miR-212-3p and miR-212-5p, when comparing stages P14 and P28. [score:4]
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Therefore, we examined the rat genome upstream from the RM2 genomic locus and we determined that a CREB dependent non-protein coding transcript that codes for the miRNAs, miRNA-212 and miRNA-132 (Vo et al., 2005) was directly adjacent to the RM2 locus. [score:2]
Dq223059 transcript contains both miR212 and miR132 between putative exon 1 and exon 2. We discovered a ∼1.6 kb and a ∼660 bp transcript that was present within ML samples that were collected 4 h post-pp-HFS. [score:1]
No PCR products were obtained using the miR-212 FP and RM2 RP. [score:1]
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Other miRNAs from this paper: rno-mir-130a, rno-mir-130b, rno-mir-132, rno-mir-152, rno-mir-184
However we only found common DNA sequence motif in the promoter region of two other upregulated miRNAs in the GK rat islets, miR-132 and miR-212 34. [score:4]
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MeCP2 controls BDNF expression and cocaine intake through homeostatic interactions with microRNA-212. [score:3]
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Other miRNAs from this paper: mmu-mir-132, mmu-mir-212, rno-mir-132
Gonadotropin-releasing hormone induces miR-132 and miR-212 to regulate cellular morphology and migration in immortalized LbetaT2 pituitary gonadotrope cells. [score:2]
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Ucar A The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagyNat. [score:2]
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For example, miR-546 and miR-710 were increased in response to cytokines whereas let-7e and miR-212-3p were more abundant in exosomes of untreated MIN6B1 cells (see Additional file 3: Figure S2B for confirmation of these results by qPCR). [score:1]
B) The level of let-7e, miR-212-3p, miR-546 and miR-710 in exosomes from MIN6B1 treated or not with cytokines for 48 h cells was determined by qPCR. [score:1]
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