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44 publications mentioning rno-mir-222

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-222. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 216
Other miRNAs from this paper: rno-mir-21, rno-mir-132, rno-mir-145, rno-mir-214, rno-mir-223
Based of our finding that PTEN expression showed down-regulation after nerve injury and thereby promoted neurite outgrowth from DRG neurons, we assumed that down-regulation of PTEN expression directly mediated miR-222-initiated neurite outgrowth from DRG neurons. [score:12]
In addition, miR-222, by targeting PTEN and tissue inhibitor of metalloproteinases-3 (TIMP3) tumor suppressors, induces tumor necrosis factor (TNF)-related apoptosis-inducing ligand resistance and enhances cellular migration through activation of the Akt pathway and metallopeptidases [28], [40]. [score:7]
The PTEN expression decreased in the soma of DRG neurons following transfection with miR-222 mimics; while the PTEN expression increased in the neurite end of DRG neurons following transfection with miR-222 inhibitor (Figure 3C). [score:7]
indicated that the miR-222 expression level significantly increased at 12 h after anisomycin treatment (Figure 5C); Western blot analysis revealed that the PTEN expression level decreased at 24 h after anisomycin treatment, and concurrently the pCREB expression level exhibited a significant increase (Figure 5D). [score:7]
In conclusion, on the basis of microarray profiling and functional analysis, we showed that miR-222, as one of the 26 differentiated miRNAs in DRG neurons after nerve injury, could regulate neurite growth by targeting PTEN, a major inhibitor of nerve regeneration. [score:6]
Our data suggested that miR-222 might probably regulate neurite growth through inhibiting the PTEN expression. [score:6]
Collectively, all data suggest that miR-222 up-regulation inhibits PTEN, maintains CREB phosphorylation, and enlarges, at least in cultured neurons, the effects of cAMP. [score:6]
Down-regulation of PTEN Expression by miR-222. [score:6]
In situ hybridization experiments performed at 4 d post injury showed that the up-regulation of miR-222 occurred mainly in DRG neurons, while miR-222 was not or weakly expressed in Schwann cells (Figure 2C). [score:6]
miR-222 gene is located on chromosome Xp11.3, and functions as an oncogene by targeting the cell cycle inhibitor p27/Kip1, thereby controlling cell proliferation [37]- [39]. [score:5]
PTEN silencing reversed the suppressive effects of miR-222 inhibitor on DRG neurons. [score:5]
A. Representative immunocytochemistry with anti-NF-200 (red) for DRG neurons, which were transfected with miR-222 mimics (miR-222), mimics control (NC), or miR-222 inhibitor (anti-miR-222), inhibitor control (anti-NC), respectively, to observe neurite outgrowth. [score:5]
In this study, we found that the pCREB level was increased in miR-222 -overexpressing DRG neurons, and the miR-222 expression level was significantly increased by c-Jun activation. [score:5]
To test this assumption, we performed transfection of miR-222 inhibitor into DRG neurons in the presence or absence of siRNA-2 against PTEN to decrease miR-222 expression. [score:5]
Our data showed that miR-222 could suppress PTEN in DRG neurons, and so we postulated that the axotomy -induced increase in miR-222 expression decreased the PTEN protein level as to promote neurite outgrowth from injured DRG neurons. [score:5]
Previous evidence shows that miR-222 post-transcriptionally regulates the PTEN expression by directly binding to the 3′-UTR of PTEN [27]. [score:5]
The results showed that there was a significant decrease in neurite outgrowth after transfected with miR-222 inhibitor alone, but a remarkable increase in the longest neurite length and total neurite length after co -transfected with miR-222 inhibitor and siRNA-2 against PTEN (Figure 4C), suggesting that PTEN might be a functional mediator for miR-222 in DRG neurons. [score:5]
To verify whether miR-222 could suppress the endogenous PTEN level, we analyzed the effects of miR-222 transfection into DRG neurons on PTEN expression. [score:5]
In addition, knocked down of PTEN by endogenous miR-222 via c-Jun activation suggested that miR-222 might be an upstream regulator of PTEN inhibition during nerve regeneration. [score:5]
Representative immunocytochemistry with anti-NF-200 (red) for DRG neurons, which were transfected with miR-222 mimics (miR-222), mimics control (NC), or miR-222 inhibitor (anti-miR-222), inhibitor control (anti-NC), respectively, to observe neurite outgrowth. [score:5]
The PTEN expression displayed the inverse time -dependent change as compared to the miR-222 expression (Figure 2C, 3A). [score:4]
miR-222 Regulates CREB Phosphorylation by Targeting PTEN to Promote Neurite Outgrowth from DRGs Neurons. [score:4]
and Western blot analysis demonstrated that overexpression of miR-222 in DRG neurons suppressed the mRNA and protein levels of PTEN by about 50% as compared to control (Figure 3B). [score:4]
In this study, we observed that after nerve injury, miR-222 was up-regulated in DRGs until 14 days. [score:4]
Several miRNAs, including miR-222 as well as miR-21 and miR-214, have been established as regulators of PTEN expression [41], [42]. [score:4]
This tendency of miR-222 up-regulation was matchable with the process of nerve regeneration, suggesting that miR-222 might trigger the intrinsic neurite growth from injured DRG neurons. [score:4]
C. showed that the treatment with anisomycin (10 µM) for 30 min induced the miR-222 up-regulation in DRG neurons. [score:4]
C. In situ hybridization with miR-222 and control scrambled probes showed up-regulation of miR-222 following axotomy and miR-222 (blue) localization in DRGs. [score:4]
PTEN was a direct target of miR-222. [score:4]
These data suggested that overexpression of miR-222 increased neurite elongation of DRG neurons and promoted their regeneration. [score:3]
Very importantly, we observed for the first time the differentially expression of miR-222 in DRGs after nerve injury. [score:3]
B. The mRNA or protein level of PTEN was down-regulated by transfection with miR-222 mimics (miR-222) as compared with that of mimics control (NC) in DRG neurons. [score:3]
We further performed immunocytochemistry to map the cellular localization of PTEN in DRG neurons following transfection with miR-222 mimics, miR-222 inhibitor, or negative control (NC) at day 3 in vitro (DIV 3). [score:3]
C. Representative micrographs following immunocytochemistry with anti-NF-200 (red) and anti-PTEN (green) showed that transfection with miR-222 reduced PTEN in the soma of DRG neurons as compared with that of NC in DRG neurons, while transfection with miR-222 inhibitor (anti-miR-222) resulted in accumulation of PTEN in the neurite end of DRG neurons as compared with that of inhibitor control (anti-NC) in DRG neurons. [score:3]
Here, we attempted to examine whether increasing intracellular cAMP and inhibition of PTEN, with miR-222 or siRNA against PTEN, could exert synergistic effects on peripheral nerve regeneration. [score:3]
Our results indicated that miR-222 definitely promoted neurite outgrowth by targeting PTEN and increasing intracellular phosphorylated CREB (pCREB) levels. [score:3]
Western blot analysis showed that the level of pCREB was up-regulated by transfection with miR-222 mimics (miR-222) as compared with that of mimics control (NC) in DRG neurons. [score:3]
Expression of miR-222 was normalized to that of RNU6B. [score:3]
Western blot analysis demonstrated that pCREB level was increased in miR-222 -overexpressing DRG neurons at DIV 3 (Figure 5A). [score:3]
In contrast, silencing of miR-222 in neurons by its inhibitor was noted to markedly impair neurite outgrowth (Figure 2A). [score:3]
We also treated DRG neurons with anisomycin, an antibiotic routinely used to activate jun-N-terminal kinase that is responsible for c-Jun activation, and then determined the miR-222 and PTEN expression levels. [score:3]
C. The neurite outgrowth from DRG neurons was observed at 72 h after transfection with miR-222 inhibitor (anti-miR-222) with or without siRNA-2. Anti-miR-222 reduced the mean longest neurite length as well as the mean total neurite length (per neuron). [score:3]
It follows that knockdown of PTEN with siRNAs induces the effects on DRG neurons similar to those induced by miR-222. [score:2]
We also noted that knockdown of PTEN by miR-222 might be synergistic with cAMP/CREB -based signaling to improve the regenerative ability of neurons, at least in vitro. [score:2]
Knockdown of PTEN Recapitulates the Effects of miR-222 on DRG Neurons. [score:2]
PTEN has been identified as a mediator of miR-222 in regulation of cell growth capacities of several cancer cell types [27], [28]. [score:2]
miR-222 is a commonly dys-regulated miRNA in many forms of cancer [35], [36]; however its function in the nervous system has not been examined. [score:2]
In addition, knockdown of PTEN by either miR-222 or siRNA-2 against PTEN for 12 h plus the ensuing 20 min stimulation of dibutyryl-cAMP (Db-cAMP) promoted neurite outgrowth from DRG neurons as compared to the above-mentioned 12-h knockdown of PTEN or the stimulation of Db-cAMP alone (Figure 5E). [score:2]
The effect of miR-222 on peripheral nerve regeneration. [score:1]
B. validation of the miR-222 level in DRGs at different time points following sciatic nerve transection. [score:1]
We further examined the possible involvement of miR-222 in CREB phosphorylation. [score:1]
A. Impact of miR-222 on CREB phosphorylation in DRG neurons. [score:1]
Knockdown of PTEN by either miR-222 or PTEN-siRNA-2 (siRNA-2) with addition of Db-cAMP (1 mM) for 20 min promoted the mean total neurite length (per DRG neuron) as compared to the stimulation of Db-cAMP alone. [score:1]
miR-222 increased neurite outgrowth from DRG neurons. [score:1]
As is known, c-Jun forms the activator protein-1 transcription factor, and is responsible for miR-222 activation in non small cell lung cancer and hepatocellular carcinoma [28]. [score:1]
Cultured neurons were subjected to transfection by either miR-222 or siRNA-2 for 12 h and then treated with or without Db-cAMP (1 mM, 20 min), followed by 24-h incubation in plain medium and fixation by 4% paraformaldehyde [5], [50], Neurite outgrowth analyses were carried out in quadruplicate. [score:1]
In the presence of siRNA-2, anti-miR-222 -mediated decrease in neurite outgrowth was abolished. [score:1]
Hybridization with DIG-labeled probes against miR-222 was carried out for 2 hours at 55°C in hybridization buffer. [score:1]
0044768.g005 Figure 5 A. Impact of miR-222 on CREB phosphorylation in DRG neurons. [score:1]
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2
[+] score: 191
Other miRNAs from this paper: rno-mir-22
We therefore propose that c-Src upregulation following traumatic stress exerts its neuroimmunomodulatory effects by upregulating miRNA222, thereby reducing PAK1 expression and downregulating IL1-β/IL1-RI signaling. [score:12]
As shown in Figure 5D, E, directed expression of c-Src in cultured neurons by transfection with adenovirus expressing constitutively active c-Src (CA c-Src) led to a marked reduction in levels of PAK1 expression and, moreover, upregulated levels of miRNA222. [score:11]
Conversely, when endogenous c-Src activity was blocked by the synthetic inhibitor PP2, miRNA222 expression was downregulated and PAK1 expression was strengthened (Figure 5B, C). [score:10]
Because PAK1 is a target for miRNA222, it is possible that c-Src modulates the PAK1-IL-1RI interaction by upregulating miRNA222 and inhibiting the expression of PAK1. [score:10]
However, the observation that the time course of miRNA222 overexpression following traumatic stress matches both the depression of PAK1 expression and immunosuppression supports the contention that PAK1 is a primary target for miRNA222 and contributes to neuroimmune modulation following traumatic stress. [score:9]
In the present paper we have shown that activation of c-Src is accompanied by strong upregulation of expression of miRNA222, an inhibitor of the immunoregulator PAK1. [score:9]
Our results suggest that neuroimmune modulation following traumatic stress is mediated by a cascade that involves c-Src -mediated enhancement of miRNA222 expression and downregulation of PAK1, which in turn impairs signaling via IL-1β/IL1-RI, leading to immunosuppression. [score:8]
We also established that PAK1 is a primary target for miRNA222, and that increased levels of miRNA222 following traumatic stress are accompanied by downregulation of PAK1 expression. [score:8]
It is therefore possible that miRNA222 upregulation is associated with c-Src signaling and that this could contribute to recovery from immunosuppression following traumatic stress (Figure 1C). [score:6]
PAK1 is a target for miRNA222, and c-Src reproducibly produced up- or downregulation of miRNA222 and PAK1. [score:6]
Functional overlap of c-Src and miRNA222 signaling has recently been demonstrated, and these factors are thought to play a joint regulatory role in tumor cell migration, nervous system development and neurodegenerative diseases [17]. [score:5]
In summary, we report that c-Src activation following traumatic stress leads to a robust increase in levels of miRNA222 and a corresponding decrease in expression of the neuromodulator PAK1, a confirmed target for miRNA222. [score:5]
These observations together suggest that c-Src is strongly upregulated by traumatic stress, and is moreover a potent regulator of miRNA222 and PAK1: it is therefore possible that changes in the levels of PAK1 following stress could in turn could be responsible for alterations in IL-1RI receptor activation following trauma. [score:5]
Also, miRNA222 is likely to have other targets in addition to PAK1, and the impact of c-Src modulation of miRNA222 expression may not be restricted to PAK1. [score:5]
To address whether PAK1 is a target for miRNA222, a miRNA222 mimetic and/or a miRNA222 inhibitor were transfected into primary cultured cortical neurons. [score:5]
Similar effects were observed at the protein level: expression of PAK1 polypeptide was decreased by the miRNA222 mimetic whereas the miRNA222 inhibitor increased PAK1 protein levels. [score:5]
Given that c-Src is strongly upregulated by traumatic stress, miRNA222 is a strong contender for the mechanistic link between c-Src activation and neuroimmune modulation following traumatic stress. [score:4]
c-Src upregulation was accompanied by marked increases in levels of miRNA222; other studied miRNAs were not affected by stress. [score:4]
Together, these observations suggest that PAK1 could be a target for regulation mediated by c-Src and miRNA222 and thereby provide a mechanistic link between c-Src signaling and IL-1β activity following traumatic stress. [score:4]
Recent studies have revealed that c-Src overlaps functionally with miRNA222, and their combined effects modulate not only cancer cell proliferation [37] but also the fine tuning of gene expression during cell differentiation and brain development [38]. [score:4]
Real-time PCR revealed that levels of miRNA222 in frontal cortex were robustly increased at day 3 following trauma, a timepoint corresponding to maximum upregulation of c-Src. [score:4]
The regulatory networks involving c-Src/miRNA222 and PAK1/IL-1RI signaling have significant potential for the development of therapeutic approaches designed to promote recovery following traumatic injury. [score:3]
As shown in Figure 6A, B, DN-c-Src resulted in a dramatic reduction in levels of miRNA222 and an equally robust increase in levels of PAK1 expression. [score:3]
Besides reported NeurimmiRs, miRNA222 has been found to play critical roles in a variety of biological processes in the central nervous system (CNS), where p21-activated kinase 1 (PAK1) is one of its targets [20, 21]. [score:3]
We therefore addressed whether modulation of c-Src activity in vivo would impact upon the expression of miRNA222 and PAK1 and on the PAK1 interaction with IL-1RI. [score:3]
CA-c-Src administration resulted in an inverse effect, leading to increased miRNA222 levels and decreased PAK1 expression. [score:3]
Extending this work, we demonstrate that, following traumatic stress, miRNA222 and PAK1 expression in frontal cortex are inversely modulated. [score:3]
As shown in Figure 2A and 2B, the miRNA222 mimetic decreased mRNA levels for PAK1; conversely, the miRNA222 inhibitor increased the levels of PAK1 mRNA. [score:3]
PAK1 is a miRNA222 target. [score:3]
The interaction between c-Src and miRNA222 expression reported here is therefore likely to play a role in orchestrating neuroimmune changes following traumatic stress. [score:3]
We therefore postulate that miRNA222 provides a mechanistic link between c-Src and immunosuppression following traumatic stress. [score:3]
PAK1 has been identified as one of the targets of miRNA222 [40, 41], a finding confirmed here. [score:3]
These data argue that c-Src is a positive regulator of miRNA222. [score:2]
In brief, 1 × 10 [6 ]neurons were transfected with 10 pmol of microRNA222 mimic and microRNA222 inhibitor. [score:2]
Homogenates of frontal cortex were prepared and assessed for microRNA222 (A) and PAK1 (B) expression using real-time PCR and western blot, respectively. [score:2]
Neurons were treated with vehicle or PP2 for 30 min, and then assessed for microRNA222 (B) and PAK 1 (C) expression using real-time PCR and western blot, respectively. [score:2]
Figure 2. Rat cortical neurons were transfected with control RNA, microRNA222 mimetic, or microRNA222 inhibitor using Lipofectamine 2000. [score:2]
c-Src plasmid, microRNA222 mimetic and microRNA222 inhibitor (Dharmacon RNA Technologies, Lafayette, CO) were transfected into primary neurons using Lipofectamine 2000 according to the manufacturer's instructions (Qiagen, Valencia, CA). [score:2]
It is well established that traumatic stress in rats leads to constitutive activation of neuroimmunomodulatory circuitry [28, 29], and we have investigated the possibility that miRNA222 regulates a feedback loop that promotes immunosuppression induced by traumatic stress. [score:2]
We conclude that PAK1 is negatively regulated by miRNA222. [score:2]
Based on the present observations, miRNA222 may act as a "negotiator" between c-Src and IL-1β signaling compartments [18]. [score:1]
Accordingly, at day 3 following trauma rats were injected icv with adenovirus expressing the dominant -negative (DN) form of c-Src, and changes in levels of miRNA222 and PAK1 were measured 72 hour later. [score:1]
Detailed analyses in cultured neurons and glial cells revealed that PAK1 -mediated enhancement of IL-1RI activation is governed to a large extent by c-Src/miRNA222 signaling; this signaling played a central role in the modulation of lymphocyte proliferation and NK cell activity. [score:1]
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3
[+] score: 74
Conversely, miR-222-3p inhibitor induced a significant increase in SOD2 protein expression (Fig.   2I, left panel) not affected by Iso treatment (Fig.   2I, right panel). [score:5]
Figure 4 Summary of expression of miR-222-3p and one of its targets SOD2. [score:5]
We then used miR-222-3p mimic and inhibitor to analyze the impact of miR-222-3p on SOD2 expression in human Cytivia plus cardiomyocytes. [score:5]
To confirm this interaction, we cloned human SOD2 3′UTR (untranslated region) harboring two potential binding sites for miR-222-3p in HEK293 cells. [score:3]
We first validated the efficiency of transfection of miR-222-3p mimic and inhibitor (not shown). [score:3]
Here, we quantified an increase in miR-222-3p expression in HF-rats, in accordance with a previous study showing an increase in miR-222 during physiological hypertrophy at cell and plasma levels [22]. [score:3]
The specific miR-222 mimic and miR-222 inhibitor and negative control were used (miRVAna, Life Technologies). [score:3]
Cotransfection of miR-222-3p mimic with human SOD2 3′UTR induced a significant decrease in luciferase expression, suggesting that miR-222-3p binds to SOD2 3′UTR (Fig.   2G). [score:3]
We observed a significantly increased expression of the 4 other miRNAs in LV, at 7 days post-MI for miR-23a-3p (Fig.   1D), at 2 months post-MI for miR-21-5p (Fig.   1D) and miR-21-3p (Fig.   1A) and at both times for miR-222-3p (Fig.   1D). [score:3]
We observed that miR-222-3p mimic induced a significant decrease in SOD2 protein expression (Fig.   2H, top panel) counteracted by Iso treatment (Fig.   2H, lower panel). [score:3]
MiR-222 mimic, miR-222 inhibitor and their negative control (100 nmol/L) were transfected with the Lipofectamine 2000 (Life Technologies) reagent (4 µL) in OptiMEM (Life Technologies). [score:3]
Our data shows the potential of miR-21-5p, miR23a-3p and miR-222-3p, and their target SOD2, as new biomarkers of post-MI HF. [score:3]
In this study, we found i) the modulation of 3 miRNAs selected in silico to interact with SOD2 in LV and plasma of the experimental rat mo del of HF and a significant increase of SOD2 in LV of 2 months post-MI rats; ii) that the circulating levels of the 3 miRNAs were differentially modulated compared to LV at 7 days post-MI, suggesting that plasma expression does not completely reflect the heart specificity at early phase of LV remo deling; iii) how miR-222-3p modulated SOD2 in hypertrophied cardiomyocytes and iv) confirmed their potential as biomarkers of cardiac remo deling in human patients phenotyped for LV remo deling post-MI with gender specificity shown by significant modulation of miR-222-3p in men and of SOD2 in women (Fig.   4). [score:2]
Interestingly, SOD2 is regulated by 5 of 13 miRNAs selected by IPA, i. e. mir-21-3p, miR-21-5p, miR-23a-3p, miR-145-5p and miR-222-3p (Fig.   1A). [score:2]
We confirmed this interaction using luciferase reporter gene assays and transfection of miR-222-3p mimic and inhibitor in human cardiomyocytes. [score:2]
miR-222-3p is a post-transcriptional regulator of SOD2. [score:2]
We also identified direct interaction between miR-222-3p, SOD2 and other molecules in the REVE-2 network at baseline (Fig.   3B, details are provided Fig.   2 and Supplementary Table  3). [score:2]
Among the 3 miRNAs identified to interact with SOD2 in our experimental rat mo del of HF, only miR-222-3p was predicted to directly interact with SOD2 in human (Fig.   2G). [score:2]
MiR-222 has been described to induce cardiomyocytes proliferation and hypertrophy and inhibit apoptosis [22]. [score:2]
Our in silico analysis suggested that only miR-222-3p directly interacts with the 3′-UTR of SOD2. [score:2]
Quantification of luciferase activity in HEK293 cells after transfection of control (white) and miR-222-3p mimic (grey) (right panel). [score:1]
To understand why the levels of the 3 miRNAS and their target, SOD2 are modulated in the same way, we analyzed deeper the REVE-2 molecular network and found an interaction of miR-222-3p with the estrogen receptor 1, located in cluster 22 and characterized by a high betweeness (0.0096), indicating a potential central role of estrogen receptor with miR-222-3p in the REVE-2 network (Supplementary Table  3). [score:1]
miR-222-3p modulation. [score:1]
Our studies based on in vivo rat experimental mo del and in vitro cardiomyocyte mo dels prompted us to assess levels of circulating SOD2 and interacting miRNAS (miR-21-5p, miR-23a-3p and miR-222-3p) in patients with high LV remo deling following MI. [score:1]
The scatter plots show the correlation between SOD2 and miR-222-3p plasma levels at 3 month post-MI for all REVE-2 population (n = 246) (left panel), for men (n = 200) (middle panel) and women (n = 46)(right panel). [score:1]
Interestingly, miR-21-5p, miR-23a-3p and miR-222-3p were significantly decreased in the plasma of 7 days MI-rats and significantly increased at 2 months post-MI (Fig.   1E) without any modulation of SOD2 in plasma of HF-rats (not shown). [score:1]
The circulating levels of miR-222-3p and SOD2 were quantified in plasma of REVE-2 patients (n = 224) respectively at baseline, 3 months, 1 year post-MI and 3 months and 1 year post-MI. [score:1]
Cells were then treated with Isoproterenol (Iso, 10 µM) in serum-free medium for 24 h and 48 h. Human SOD2 3′UTR (824 bp) harboring two potential binding sites for miR-222-3p was cloned into SpeI and HindIII cloning site of pMIR-REPORT vector (Ambion). [score:1]
The resulting construct (20 ng) was co -transfected with control mirVana mimic or mirVana mimic miR-222-3p (each 30 nM, ThermoFisher Scientific) and 20 ng of β-galactosidase control plasmid (Promega) into 48well-plated HEK293 reporter cells by the use of Lipofectamine 2000 (Invitrogen). [score:1]
Here, we focused on 3 miRNAs, miR-21-5p, miR-23a-3p and miR-222-3p and their target SOD2, detected in plasma that we characterized for their potential as biomarkers of HF. [score:1]
Conversely, the significant increase of circulating levels of miR-222-3p is only found in men at 3 months post-MI (Fig.   3C, right panel). [score:1]
Interestingly, the REVE-2 molecular network previously built with 23 circulating molecules quantified in blood samples of REVE-2 patients, shows that these 3 miRNAs were highly central molecules with the highest betweeness centrality for miR-21-5p and miR-222-3p [17], indicating that they are crucial molecules to maintain functionality and coherence of signaling mechanisms in the REVE-2 network. [score:1]
In this study, we showed for the first time, that levels of circulating miR-21-5p, miR-23a-3p and miR-222-3p decrease in patients with high remo deling at baseline and increase at 3 months post-MI. [score:1]
Detailed information are provided as Fig.   2 and Supplementary Table  3. (C) Quantification by RT-qPCR of miR-222-3p in plasma extracted from REVE-2 patients at baseline and after 3 months and 1 year post-MI for all the population (left panel). [score:1]
miR-222-3p and SOD2 were quantified in LV and plasma of experimental mo del of MI rat at 7 days (n = 9) and 2 months (n = 9) after MI (n = 18) or sham (n = 18) surgery. [score:1]
Moreover, we observed a significant correlation between circulating levels of SOD2 and of miR-222-3p quantified at 3 months post-MI in the whole REVE-2 population and men population but not in women population (Fig.   3D). [score:1]
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4
[+] score: 46
Other miRNAs from this paper: rno-mir-221
We found that SOCS1 overexpression in BRL cells reduces Met expression (Fig.   3D) and induces a dramatic decrease in miR-221 and miR-222 expression (Fig.   3E). [score:7]
As expected, SOCS1 RNA interference knockdown in rat hepatocytes showed a prominent increase of miR-221 and miR-222 expression (Fig.   3F). [score:4]
Because Met activation by growth factors can enhance miR-221 and miR-222 expression, we investigated the possibility that indirectly evaluation of SOCS1 expression levels by examining miR-221 and miR-222 expression may predict AOC patient prognosis. [score:4]
Circulating miR-221 and miR-222, which are indirectly regulated by SOCS1, may be potential serological biomarkers for predicting the outcome for patients with acute obstructive cholangitis. [score:3]
We found that circulating miR-221 and miR-222 levels also were inversely correlated with SOCS1 expression in the liver (R = −0.606 and −0.512, respectively; Fig.   4A and B). [score:3]
Furthermore, Pearson’s correlation analysis also showed that miR-221 and miR-222 in serum had an inverse correlation with SOCS1 expression, which is similar to the results in liver tissue. [score:3]
Thus, we examined miR-221 and miR-222 expression in our study. [score:3]
The results suggested that lower expression of circulating miR-221 and miR-222 after ENBD was associated with delayed restoration of liver function. [score:3]
However, SOCS1 expression in BRL cells did not show the expected significant decrease after transfection with miR-221 or miR-222 (Fig.   4E), which may be because of LPS stimulation or the difference between human SOCS1 and rat SOCS1. [score:3]
Previous studies reported that Met is able to enhance miR-221 and miR-222 expression 17, 21. [score:3]
Given that both miR-221 and miR-222 have the same sequences in humans and rats, we also explored the potential correlation between circulating miR-221/222 and prognosis of AOC patients. [score:1]
This suggests that circulating miR-221 and miR-222 are potential biomarkers to predict the AOC prognosis in the rat. [score:1]
Circulating miR-221 and miR-222 are potential biomarkers to predict acute obstructive cholangitis prognosis. [score:1]
Both miR-221 and miR-222 had a statistically significant inverse correlation with SOCS1 (R = −0.687 and −0.632, respectively; Fig.   3G and H). [score:1]
Circulating miRNA is easy to detect, and we examined circulating miR-221 and miR-222 levels in rat serum. [score:1]
Meanwhile, miR-222 increased significantly in both BDL and AOC groups (Fig.   3B). [score:1]
Other RNA oligonucleotides (including miR-221, anti-miR-221, miR-222, anti-miR-222, miR control and siRNA control) was also obtained from RiboBio. [score:1]
Interestingly, comparing the results between two groups, both miR-221 and miR-222 in the bad recovery group were significantly lower than those in the good recovery group (Fig.   4D). [score:1]
This indicates that circulating miR-221 and miR-222 levels are associated with AOC prognosis in rats and in humans. [score:1]
Figure 4Circulating miR-221 and miR-222 are potential biomarkers to predict acute obstructive cholangitis prognosis. [score:1]
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5
[+] score: 39
The mRNA encoding the cyclin dependent kinase inhibitor 1c (Cdkn1c) was up-regulated 3-fold in E13 ENPs and is predicted to be targeted by three miRNAs that were down-regulated: miR-92, miR-222, and miR-363-3p. [score:11]
Notably, we found miR-222, miR-291-3p, miR-183, miR-363-3p, miR-92, miR-19a and miR-145 as down-regulated miRNAs between E11 and E13 and whose expression was negatively correlated with the expression of their predicted targets. [score:10]
Additional support for this hypothesis was provided by the miRNA-TF mRNA network analysis in Figure 8. We found four down-regulated miRNAs (miR-92, miR-183, miR-222 and miR-291-3p) that were predicted to target multiple TFs, which were up-regulated in E13 ENPs. [score:9]
Focusing on the down-regulated miRNAs that had a significant negative correlation in Figure 6, we performed network analysis and identified miR-92, miR-183, miR-222 and miR-291-3p as predicted to target multiple TFs that were up-regulated in E13 ENPs (Figure 8). [score:9]
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6
[+] score: 34
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
In breast cancer cells, over -expression of miR-221, miR-222, let-7 and miR-20b is associated with reduced of ERα protein content, signaling and expression of ERα target genes [47- 49]. [score:7]
Ovarian follicle expression of miR-221 and miR-222 has been reported to be repressed by androgens [42- 44] which regulates cell proliferation by targeting p27/kip1 [44, 45]. [score:6]
In the cystic follicle, expression of miR-222 becomes restricted to theca only, suggesting that miR-222 modulates AR expression and hereby paracrine regulation. [score:6]
In situ localization shows specific expression of miR-222 in the theca cells (Figure  5) where it may be involved in regulation of the ERα. [score:4]
A list of differentially expressed miRNAs (Fold change ≥ 2 and their corresponding P value) is presented in Figure  4. Beside this group, miRNAs which were also highly abundant in DHT -treated ovaries are rno-miR-221, rno-miR-222, rno-miR-25, rno-miR-26b, rno-miR-379*, rno-let-7d, rno-miR-24, rno-miR-673, rno-miR-26b, rno-miR-335, rno-miR-382*, rno-miR-412, rno-miR-99a*, rno-miR-543, rno-miR-674-3p, rno-miR-409-3p. [score:3]
For example, rno-miR-96, rno-miR-31 and rno-miR-222 were exclusively expressed in the theca of cystic follicles. [score:3]
Here we observed higher expression of miR-222 in the DHT -induced PCOS rats, a response most evidenced in both theca and granulosa of early stage follicles. [score:3]
These include rno-miR-195, rno-miR-125a-5p, rno-let-7a, rno-miR-16, rno-miR-30b-5p, rno-let-7c, rno-let-7b, rno-miR-125b-5p, rno-miR-221, rno-miR-222, rno-miR-26a, rno-miR-322, rno-miR-23a, rno-miR-191, rno-miR-30 family, rno-miR-21, rno-miR-126, rno-miR-23b, rno-miR-145 and rno-miR-494. [score:1]
These included rno-miR-24, rno-miR-31, rno-miR-96, rno-miR-183, rno-miR-222, rno-miR-489, U6 snRNA (positive control) and scrambled miRNA (negative control). [score:1]
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7
[+] 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-212, rno-mir-181a-1, 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
These miRNAs were chosen as representative of the different patterns that were observed: up-regulation (miR-21-5p) or down-regulation (miR-222-3p) during latency; up-regulation (miR-181c-5p) or down-regulation (miR-500-3p) in the chronic period; up-regulation (miR-146a-5p) or down-regulation (miR-551b-3p) in the entire course of the disease. [score:21]
Another subgroup of miRNAs displayed an opposite pattern, i. e. decreased expression during latency: miR-7a-1-3p, miR-107-3p, miR-138-5p, miR-139-3p, miR-186-5p, miR-204-5p, miR-222-3p, miR-324-3p and miR-505-3p were significantly decreased during latency (peak at 4 days after SE), then gradually returned to control levels (Fig. 2, Supplementary Fig. S2). [score:3]
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8
[+] score: 22
As such, the translational regulation of ESR1 represents another remarkable functional cross-talk between miRNAs, which we show to be expressed in a mutually exclusive manner between the cerebellum (miR-206) and the hippocampus/amygdaloid regions (miR-221/miR-222). [score:6]
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]
Accumulations of miR-497 in the cerebellum, of miR-7 in the hypothalamus, and of miR-221 and miR-222 in the hippocampus have also been described in mice [39] and zebrafish (larval and adult brain), where miR-222 is expressed in specific groups of differentiating cells in the rostral parts of the brain [42]. [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]
Indeed, the overlapping expression patterns of miR-222 in zebrafish, mice and rats suggest that this miRNA is important for some specialized hippocampal functions. [score:3]
The most pronounced differences in expression patterns among these nine miRNAs were seen for the miR-221 family members (miR-221 and miR-222), which showed a cerebellar reduction of more than 60-fold compared to the hippocampus and the amygdaloid region. [score:2]
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[+] score: 21
More importantly, the miRNAs analyzed in this study not only included the miRNAs like Let-7a, miR-15b, miR24, miR-100 and miR-125 which may suppress the expression of cyclins A and B, and miRNAs such as Let-7a, miR24 and miR-125 which may regulate activity of CDK1, but also miRNAs such as miR-181a, miR-221 and miR-222 which can target CDK inhibitors [30– 32]. [score:10]
To investigate whether miRNAs have a role in the cell cycle regulation of splenocytes following aniline exposure, the expression of miRNAs, including Let-7a, miR-15b, miR24, miR-100, miR-125, miR-181a, miR-221 and miR-222 which are known to mainly control G2/M phase regulators [30– 32], was analyzed by using real-time PCR and the results are presented in Fig 7. Aniline exposure led to significantly decreased expression of Let-7a (decreased 82%), miR-15b (decreased 62%), miR24 (decreased 78%), miR-100 (decreased 63%), miR-125 (decreased 86%), whereas miR-181a, miR-221 and miR-222 increased by 155%, 78% and 56%, respectively, in comparison to controls (Fig 7). [score:5]
Real-time PCR analysis of miRNAs Let-7a, miR-15b, miR24, miR-100 and miR-125 (A), and miRNAs miR-181a, miR-221 and miR-222 (B) expression in rat spleens following aniline exposure. [score:3]
Therefore, greater decreases in Let-7a, miR-15b, miR24, miR-100 and miR-125 expression and significant increases in miR-181a, miR-221 and miR-222 levels in the spleens following aniline treatment may be mechanistically important in generalizing that aniline exposure leads to increased cyclin A, cyclin B, CDK1, and decreased p21, p27, thus triggering the splenocytes to go through G2/M transition. [score:3]
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10
[+] score: 19
Since it has been demonstrated that miR-222 can target p27 [kip1], a critical regulator of cell cycle (49), and the phosphatase 2A subunit B (PPP2R2A), which inhibits Akt phosphorylation (48), we can assess that HMGA overexpression contributes to NSCLC progression by dysregulating cell cycle and Akt signaling (48) (Figure 1B). [score:9]
Indeed, it has been reported that at least HMGA1 is able to directly regulate the expression of miR-222 in NSCLC cells (48). [score:5]
HMGA1 is able to induce the expression of miR-222, which in turn can target p27 [kip1] and PPP2R2A, then activating the AKT signaling. [score:5]
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11
[+] score: 17
Other miRNAs from this paper: hsa-mir-221, hsa-mir-222, rno-mir-221
While miR-222 RNA was also downregulated in the aortas of Tg rats, the reduced level of expression was not significant compared to controls. [score:5]
Overexpression of miR-221 or miR-222 inhibits monocyte adhesion induced by Tat in HUVECs. [score:5]
Intriguingly, homogenates of the aorta and heart also demonstrated increased expression of ICAM-1 when assessed by real-time RT-PCR and Western blot as shown in Figs. 7B and C. Furthermore, consistent with the in vitro findings, expression of miR-221, but not miR-222, was decreased in aorta isolated from HIV Tg rats, compared with the WT rats (Fig. 7D). [score:4]
0060170.g006 Figure 6Transfection of HUVECs with miR-221 or miR-222 precursor abrogated Tat -induced monocyte adhesion. [score:1]
HUVECs transfected with miR-221 or miR-222 precursor or a precursor control for 24 h were exposed to Tat (14.4 nM) for 12 h followed by western blot analysis for ICAM-1. All the data are presented as mean ± SD of three independent experiments. [score:1]
Transfection of HUVECs with miR-221 or miR-222 precursor abrogated Tat -induced monocyte adhesion. [score:1]
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12
[+] score: 16
Other miRNAs from this paper: rno-mir-221
Recently, it became apparent that microRNAs, especially miRNA-221 and miRNA-222, may be important inhibitors of Kip1 translation (Galardi et al., 2007; Martínez-Sánchez and Gebauer, 2010). [score:5]
miR-221 and miR-222 expression affects the proliferation potential of human prostate carcinoma cell lines by targeting p27Kip1. [score:5]
Data are expressed as ΔΔCt values for miRNA221 (A) or miRNA222 (B) using 4.5 S -RNA (diamonds), U6-snRNA (squares), or β-actin mRNA (full circles) as internal standards. [score:3]
We could, however, not find any obvious changes in miRNA-221 or miRNA-222 in residual liver tissue over the entire experimental period (Figure 7) indicating that these microRNAs do not contribute to the regulation of Kip1 abundance in residual liver tissue upon PH. [score:2]
Figure 7 Abundances of miRNA221 or miRNA222 in total RNA preparations from rat liver during or at different times after partial hepatectomy as determined by qPCR. [score:1]
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13
[+] score: 11
12 of these miRNAs were ≥50% up-regulated in both groups with particularly strong increases in expression for miR-199a, miR-21, miR-214, miR-221, miR-222, and miR-31 (Figure 2B). [score:6]
Several miRNAs, including miR-21, miR-27, miR-31, miR-199a, miR-214 and miR-222 were up-regulated in these mouse mo dels in the same directions and to similar extents as observed in this study [11], [18]. [score:5]
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[+] score: 10
Astrocytes activated with LPS and INF- γ showed upregulation of miR-222 [13]. [score:4]
MiRNA-221 and miRNA-222 were upregulated in the activated astrocytes. [score:4]
MiRNA-221 and miRNA-222 are two highly homologous miRNAs, whose dysregulations have been recently described in several types of human tumors. [score:2]
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[+] score: 10
Other miRNAs from this paper: rno-mir-126a, rno-mir-126b, rno-let-7g
Even though its overexpression in endothelial cells seems to inhibit angiogenesis, in cardiac tissue miR-222 has been reported to modulate important physiological function in cardiac stem cells, as well as in conferring protection against adverse remo deling (e. g. decreased cardiac fibrosis) and dysfunction after heart injury 31, 32. [score:5]
Ding S Huang H Xu Y Zhu H Zhong C MiR-222 in Cardiovascular Diseases: Physiology and PathologyBiomed. [score:2]
For analysis of miRNA expression, the following commercial kits were used: mirVana miRNA isolation Kit (Invitrogen), TaqMan Advanced miRNA cDNA Synthesis Kit (Applied Biosystems) and the TaqMan Advanced miRNA Assays: rno-miR-126-3p, rno-miR-126-5p, rno-miR-222-3p and rno-let-7g-5p. [score:2]
Another important miRNA with validated role in angiogenesis is miR-222. [score:1]
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16
[+] score: 9
As shown in Figure 1E, F, miR-153 expression was elevated and miR-222 expression was decreased at 24 hours post-CCI; expression of both miR-135a and miR-135b was reduced at 7 days post-CCI; miR-124 expression was comparable in control and CCI samples at both the 24-hour and 7-day time points. [score:9]
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[+] score: 8
Other miRNAs from this paper: rno-mir-219a-1, rno-mir-219a-2, rno-mir-219b
This local protein synthesis is finely controlled by microRNAs, such as miR-222. [score:1]
Enhanced regeneration of aligned neurofilaments (NF [+], red) within nanofibers-hydrogel scaffolds that incorporated miR-222 at 10 days post-implantation. [score:1]
First, Cy5-labeled oligonucleotides (ODN), 488-ODN, NEG-miR (100 μM) or miR-222 was complexed with MNP (2.0 mg/ml) at room temperature for 10 minutes. [score:1]
Given this knowledge gap, we next closely examined the efficacy of scaffold -mediated miR-222 delivery in supporting in vivo axon regeneration. [score:1]
As shown in Fig. 6B, after 10 days post-implantation, robust neurite ingrowth was observed in PCLEEP-collagen hybrid scaffolds that incorporated miR-222. [score:1]
However, there is no study on miR-222′s effects on SCI treatment to date. [score:1]
Taken together, these results demonstrate the efficacy of our scaffolds in providing effective non-viral delivery of bioactive miR-222 to promote nerve regeneration after SCI. [score:1]
In addition, nerve regeneration may be further assisted by the synergistic supplementation of biomoleucles such as neurotrophic factors (e. g. NT-3) and microRNAs (e. g. miR-222). [score:1]
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[+] score: 7
Down-regulation of Dicer1, predicted by miR-152, miR-203 and miR-222, could be a part of a complex regulation related to the global abundance of miRNAs and their requirements for processes such as cell-cycle exit control and onset of cell differentiation. [score:5]
Similar analysis of “late” group, including c-Maf, Ets1, N-Myc, Nfat5, and Nfib, yielded 10 miRNAs: miR-20b, miR-145, miR-152, miR-155, miR-181a, miR-203, miR-222, miR-301a, miR-324-5p, and miR-351, with multiple connections. [score:1]
Ten miRNAs, miR-20b, miR-145, miR-152, miR-155, miR-181a, miR-203, miR-222, miR-301a, miR-324-5p, and miR-351. [score:1]
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[+] score: 7
By targeting the PTEN gene, mir-222 has been shown to promote neurite outgrowth (34). [score:3]
Of those, 9 miRNAs (let-7c-1, miR-221-3p, miR-221-5p, miR-222-3p, mir-322-2, mir-34c, miR-384-5p, mir-496, and mir-542-1) reported consistent directional changes as our data (15, 31– 33). [score:2]
Most importantly, two of these microRNAs (miR-222-3p and miR-384-5p) were also found to be reversed in the amygdala after social enrichment (Table 3). [score:1]
These include precursor miRNAs mir-204 and mir-299a as well as mature miRNAs miR384-5p, miR-222-3p, and miR-301b-3p. [score:1]
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[+] score: 7
Those miRNAs, we call them the epi-miRNAs, includes, for example, miR-148a, miR152, miR222 that targets mRNA of DNMTs and leads to re -expression of hyper-methylated tumor suppressors [32]. [score:7]
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[+] score: 7
In addition, 6 miRNA downregulated in our analyses (miR-26a, 29a/b/c, 222, and 383, Additional file 4: Table S1) are predicted to bind 3′UTR of Dnmt3B, with miR-222, miR-383 and miR-29b have demonstrated to directly affect Dnmt3B expression [49, 50]. [score:7]
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[+] score: 7
For liver cancer, one recent study reported that miR-21, miR-31, miR-122, miR-221, miR-222 were significantly up-regulated in HCC tissues, whereas miR-145, miR-146a, miR-200c, and miR-223 were found to be down-regulated [15]. [score:7]
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23
[+] score: 6
Other miRNAs from this paper: rno-mir-221, rno-mir-224
In the light of the above findings, and as demonstrated for other miRNAs, such as miR-221 and miR-222 [35- 37], miR-224 seems to have a dual mode of action that depends on the type of cancer involved: it acts as an onco-miR in some cancers and as an oncosuppressor-miR in others, suggesting that different molecular targets and networks are regulated by miR-224 in different neoplastic scenarios. [score:6]
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24
[+] score: 6
Similarly, TargetScan analysis identified the following miRNAs that are conserved in humans and are predicted to influence the NT3 gene: miR-21-5p, miR-222-3p, and miR-221-3p. [score:3]
Both miR-222-3p and miR-221-3p share the same seed sequence (AUGUAGCA). [score:1]
MicroRNAs predicted to influence neurotrophins: a BDNF (miR-206-3p, miR-10a-5p, miR-1b, miR-195-5p and miR-497-5p), b NT3 (miR-21-5p, miR-222-3p and miR-221-3p), and c NGF (let-7b-5p and miR-98-5p) were quantified by qPCR analysis in YA (n = 8) vs VO (n = 10) rat vastus lateralis muscle and WT (n = 8) vs Sarco (n = 7) gastrocnemius muscle. [score:1]
In contrast to the aforementioned studies in aging muscle, most of the miRNAs studied herein have been examined in the context of experimental denervation, including miR-206 (increases after reinnervation), miR-10a-5p (increases four- to seven-fold with denervation), miR-1 (increases up to 10-fold following denervation and remains elevated after reinnervation), miR-195 (increases up to 10-fold with denervation), miR-21 (increases with denervation), miR-221 (no consistent change), miR-222 (no consistent change), and miR-98 (increases up to 10-fold with denervation) [43, 47, 48]. [score:1]
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25
[+] score: 6
Other miRNAs from this paper: rno-mir-15b, bta-mir-222, bta-mir-15b
It has been demonstrated that dietary supplementation of ARG or NCG affect microRNAs (miR-15b, miR-222) targeting VEGFA and endothelial NO synthase gene expressions in umbilical vein, consequently regulate the function and volume of the umbilical vein, provide more nutrients and oxygen from the maternal to the fetus tissue [36]. [score:6]
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[+] score: 5
Among these differentially expressed miRNAs, rno-miR-130b-3p, rno-miR-132-3p, rno-miR-181a-1-3p, rno-miR-222-3p, rno-miR-351-5p, and rno-miR-21-3p had the largest positive fold changes, while rno-miR-335, rno-miR-192-3p, rno-miR-194-5p, rno-miR-192-5p, rno-miR-499-5p, and rno-miR-210-3p had the largest negative fold changes (Table 1). [score:3]
Relative expression levels of the selected miRNAs and mRNAs were depicted in Figure 3. Consistent with the microarray data, real-time PCR confirmed that, compared with controls, rno-miR-132-3p, rno-miR-181a-1-3p, rno-miR-222-3p, and rno-miR-351-5p were significantly increased, while rno-miR-192-3p, rno-miR-194-5p, rno-miR-29c-3p, rno-miR-185-5p, and rno-miR-30c-5p were significantly decreased in stone-forming rat kidneys. [score:2]
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[+] score: 5
Emerging evidence indicates that miRNAs act as key modulators of target gene expression, and some, such as miR-21, miR-126, miR-33, miR-125, and miR-222, have been shown to be involved in the pathogenesis of stroke [5, 6]. [score:5]
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[+] score: 5
Notably, cardiac-specific miR-1, miR-133, miR-208 and miR-499 were all suppressed by two or more orders of magnitude [34], [35], as were the stemness and cell cycle repressors miR-141 and miR-137 [36]; in contrast, the proliferative miRNAs, miR-222 [37], increased dramatically in MDCs, and miR-221 was undetectable in myocytes but highly expressed in MDCs (Figure 5D). [score:5]
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29
[+] score: 4
Several miRNAs are demonstrated that associated with OA development and modulation such as miR-18a (chondrocyte differentiation), miR-27b (controlling the expression of MMP-13), miR-34a (prevention of cartilage degradation), miR-140 and miR-222 (controlling cartilage homeostasis), miR-146 (promotion of inflammatory OA), miR146a (OA cartilage pathogenesis), miR-675 (cartilage repair) [30, 31]. [score:4]
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30
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Similarly, within the differentially expressed pool of miRNAs, 10 were identified that are intimately involved in regulating intracellular trafficking pathways, including: miR-7b-5p, miR-9-5p, miR-31-5p, miR-92a-3p, miR-106-5p, miR-126-3p, miR-150-5p, miR-204-5p, miR-222-3p, and miR-322-5p (S2 Fig). [score:4]
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[+] score: 3
Other miRNAs from this paper: rno-mir-221
miR-221 and miR-222 promote Schwann cell proliferation and migration by targeting LASS2 after sciatic nerve injury. [score:3]
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[+] score: 3
In addition, miR-222 was postulated as a potential regulator of the articular cartilage mechanotransduction pathway, since its expression patterns in articular cartilage are higher in the weight-bearing anterior medial condyle as compared with the posterior nonweight-bearing medial condyle [34]. [score:3]
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[+] score: 3
miR-221 and miR-222 promote Schwann cell proliferation and migration by targeting LASS2 after sciatic nerve injury. [score:3]
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34
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-99a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-146a, mmu-mir-129-1, mmu-mir-206, hsa-mir-129-1, hsa-mir-148a, mmu-mir-122, mmu-mir-143, hsa-mir-139, hsa-mir-221, hsa-mir-222, hsa-mir-223, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-146a, hsa-mir-206, mmu-mir-148a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, rno-let-7d, rno-mir-335, rno-mir-129-2, rno-mir-20a, mmu-mir-107, mmu-mir-17, mmu-mir-139, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-125b-1, hsa-mir-26a-2, hsa-mir-335, mmu-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-17-1, rno-mir-18a, rno-mir-21, rno-mir-22, rno-mir-26a, rno-mir-99a, rno-mir-101a, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-127, rno-mir-129-1, rno-mir-139, rno-mir-143, rno-mir-145, rno-mir-146a, rno-mir-206, rno-mir-221, rno-mir-223, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-486-1, hsa-mir-499a, mmu-mir-486a, mmu-mir-20b, rno-mir-20b, rno-mir-499, mmu-mir-499, mmu-mir-708, hsa-mir-708, rno-mir-17-2, rno-mir-708, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-486b, rno-mir-126b, hsa-mir-451b, hsa-mir-499b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-130c, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, hsa-mir-486-2, mmu-mir-129b, mmu-mir-126b, rno-let-7g, rno-mir-148a, rno-mir-196b-2, rno-mir-486
Two miR-221 and miR-222 seed elements were identified in the 3’UTR of ERα and transfection of miR-221 and miR-222 suppressed ERα protein, but not mRNA in ERα positive MCF-7 and T47D cells. [score:3]
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35
[+] score: 3
Yu B miR-221 and miR-222 promote Schwann cell proliferation and migration by targeting LASS2 after sciatic nerve injuryJ. [score:3]
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36
[+] score: 3
For example, miR-195, miR-497, and miR-30b were found to be enriched in the cerebellum whereas miR-218, miR-221, miR-222, miR-26a, miR-128a/b, miR-138 and let-7c were highly expressed in the HIP. [score:3]
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[+] score: 3
microRNA-222 targeting PTEN promotes neurite outgrowth from adult dorsal root ganglion neurons following sciatic nerve transection. [score:3]
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38
[+] score: 2
Other miRNAs from this paper: mmu-mir-221, mmu-mir-222, rno-mir-221
MIR221/MIR222 -driven post-transcriptional regulation of P27KIP1 and P57KIP2 is crucial for high-glucose- and AGE -mediated vascular cell damage. [score:2]
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[+] score: 2
Forrest AR Induction of microRNAs, mir-155, mir-222, mir-424 and mir-503, promotes monocytic differentiation through combinatorial regulationLeukemia. [score:2]
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40
[+] score: 1
miR-145, miR-221, and miR-222 were selected based on their relationship with miR-143 and miR-223, respectively. [score:1]
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41
[+] score: 1
Some miRNAs, including miR-1, miR-145, miR-122, miR-221, and miR-222, have been linked to vascular endothelial dysfunction [12]. [score:1]
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[+] score: 1
MicroRNA profiling identified several miRNAs that have been previously associated with cardiac hypertrophy such as miR-214, miR-23b, miR-15b, rno-miR-26b, rno-miR-221, rno-miR-222, rno-miR-107 [59], miR-23a, miR-208, rno-miR-133b, miR-19a and mi-r133a [60]. [score:1]
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[+] score: 1
Moreover, miR-222/223 enriched in the MSC-EVs vs CDC-EVs in our study, was implicated in inducing dormancy and prolonged survival of breast cancer cells together with increased drug resistance [49]. [score:1]
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44
[+] score: 1
On the other hand, both EEP and Pn significantly inhibited in a dose -dependent manner the activation of HIF1 α. Finally, VEGF mRNA and microRNAs associated with angiogenesis in previous studies (miR-126, miR-19b, miR-221, miR-222, miR-27b, and miR-17) were evaluated by real-time PCR. [score:1]
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