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14 publications mentioning rno-mir-326

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-326. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 169
In hippocampal neurons, miRNA overexpression inhibits endogenous Arc protein expression in response to BDNF, while inhibition of miR-326 facilitates Arc mRNA expression. [score:11]
In terms of regulation of mRNA stability versus translation, we show that inhibition of miR-326 in unstimulated neurons enhances Arc mRNA expression without affecting protein, indicating that miR-326 may specifically function to destabilize Arc mRNA. [score:8]
Co -expression of miR-34a with miR-19a, miR-378, or miR-326 did not modulate the inhibition induced by miR-34a expression alone. [score:7]
Using the wildtype Arc 3′UTR, we independently confirmed inhibition of reporter expression by the candidates selected from Figure 1A and further demonstrated inhibition by miR-19a and miR-326 (Figure 2A). [score:7]
A significant difference in luciferase expression was observed after substitution mutation or deletion of the miRNA binding sites for miR-19a, miR-34a and miR-326 in response to expression of the respective miRNAs, relative to the wildtype Arc 3′UTR. [score:6]
miR-34a, miR-326 and miR-193a downregulate Arc protein expression in cultured hippocampal neurons. [score:6]
In contrast, Arc -regulating miR-34a, miR-326, miR-19 and miR-193a were not significantly regulated, although there was trend for miR-34a upregulation at 30 minutes post-BDNF (p = 0.07). [score:6]
miR-34a and miR-326 were expressed alone and in combination with other Arc -targeting miRNAs. [score:5]
Inhibition of the Arc 3′UTR by miR-326 was not affected by co-transfection with miR-19a, yet significantly stronger inhibition was obtained when miR-326 was paired with miR-193a or miR-378. [score:5]
Ectopic expression of miR-193a, miR-326, and miR-34a all enhanced BDNF-evoked Arc protein expression. [score:5]
TargetScan further predicts a binding site for miR-326 in two dendritically expressed RNAs with roles in synaptic plasticity, protein kinase C-zeta and tissue plasminogen activator. [score:5]
In situ hybridization confirms miRNA expression in adult dentate granule cells and hippocampal pyramidal cells, while qPCR analysis shows enhanced expression of miR-19a, miR-34a, and miR-326 in synaptoneurosomes relative to cell body restricted, small nucleolar RNA. [score:5]
SDM of the proximal miR-326 site (site S2 in Figure 1C) did not affect the luciferase activity (data not shown) whereas mutations directed to the second site resulted in a modest 0.3-fold enhancement in expression relative to wildtype. [score:5]
Triplet substitution mutation of the distal miR-326 site (S4), deletion of S4, or deletion of S2 failed to enhance expression relative to wildtype control significantly (Figure 2C). [score:4]
A significant downregulation of Arc protein was seen in miR-193a and miR-326 transfected cells. [score:4]
miR-34a, miR-326, and 193a downregulate Arc protein in hippocampal neurons. [score:4]
Introducing three point mutations in the binding seed resulted in partial but significant rescue of luciferase expression for miR-34a and miR-326 (Figure 2A). [score:4]
miR-326 is expressed in neurons and works in a feedback loop with Notch during development of the nervous system [74]. [score:4]
Mutations in the seed region of three miRNAs (miR-34a, miR-326, and miR-19a) partially or fully rescue reporter expression. [score:4]
Thus, miR-34a and miR-326 have Arc and Notch as common targets. [score:3]
miR-19a and miR-326 were added to this analysis because TargetScan (Release 6.0; November, 2011) shows a vertebrate-conserved binding site for miR-19a and two binding sites for miR-326 in the Arc 3′UTR. [score:3]
However, significant recovery of expression was obtained when both miR-326 binding sites were deleted. [score:3]
Prominent miR-34a and miR-326 expression was observed in the cell body layers of the dentate gyrus and hippocampus proper. [score:3]
Regulation of Arc by miR-34 and miR-326 is attenuated by point mutations and deletion of the microRNA seed region. [score:3]
Inhibition of the perfectly matched miR-326 sensor was 70% of control, approximately equal to effects obtained with the wildtype Arc 3′UTR reporter. [score:3]
Thus, at DIV10, expression of miR-19a, miR-34a, miR-326 and miR-193a were decreased while Arc mRNA was elevated. [score:3]
After 7 days in vitro (DIV7), neurons were transfected with plasmids expressing DsRed only (empty vector), ds-Red-miR-150, DsRed-miR-326 or DsRed-miR-193a using Lipofectamine-2000 Reagent (Invitrogen). [score:3]
After day 10, the expression of the miRNAs increased, though levels of miR-326 remained significantly decreased relative to DIV3. [score:3]
We chose to study miR-34a and miR-326 as strong candidates from the point mutation analysis and miR-193a because of its synergistic effects. [score:2]
miR-326 and miR-193a experiments were similarly analyzed but in this series mean values of cytoplasmic pixels from the 20 highest DsRed expressing cells were compared with the 20 lowest. [score:2]
Collating results from mutation studies in HEK cells with effects of miRNA manipulation in hippocampal neurons, we provide evidence that miR-19a, miR-34a, miR-193a, and miR-326 are capable of modulating Arc. [score:2]
Dramatic changes in mature miR-19a, miR-34a, miR-326 and miR-193a were observed during development, with maximum changes of more than 100-fold. [score:2]
In contrast, miR-19a, miR-34a, miR-326 and miR-193a were not significantly regulated. [score:2]
C) Whereas mutation of the distal (S4) miR-326 site or deletion of either site individually had only minor effects, the deletion of both sites at the same time gave full recovery of luciferase activity. [score:2]
The following combinations: miR-34a/miR-193a, miR-326/378 and miR-326/193a gave enhanced inhibition of luciferase activity compared to miR-34a and miR-326 alone. [score:2]
Interestingly miR-19, miR-34 and miR-326 are all dysregulated in multiple sclerosis patients [62]. [score:2]
We confirmed that PNA-AS transfection almost completely eliminated PCR-detectable miR-326, miR-34a and miR-193 (Figure 5B). [score:1]
The effects of miR-19a and miR-34a and miR-326 is dependent on intact microRNA binding sites. [score:1]
While little is currently known about mir-193a and miR-19a, new studies have shed light on miR-34 and miR-326 function in the nervous system. [score:1]
The microRNAs included were miR-19a, miR-34a, miR-193a and miR-326. [score:1]
B) Quantitative relative real-time PCR of miR-19a, miR-34a, miR-326, miR-193a and miR-132. [score:1]
0041688.g004 Figure 4 Cultured hippocampal neurons were transfected with either empty vector-DsRed, miR150-DsRed, miR34a-DsRed, miR326-DsRed or miR193a-DsRed. [score:1]
Mean Arc levels were comparable between cells transfected with empty vector and miR-150 controls, but were significantly reduced in neurons transfected with miR-34a, miR-326, or miR-193a (Figure 4C and E). [score:1]
For miR-326 and miR-193a, CellProfiler threshold detection was used to separate the nuclear and cytoplasmic signals. [score:1]
B) miRNA in situ hybridization was performed on coronal hippocampal sections using LNA probes for miR-326, miR-34a, and scrambled control. [score:1]
D) representative images of cells transfected with miR-326-DsRed (cells labelled with DsRed and red arrows) and non -transfected cells (white arrows). [score:1]
B) Quantitative relative real-time PCR of miR- miR-133, 19a, miR-34a, miR-326 and miR-193a. [score:1]
Cultured hippocampal neurons were transfected with either empty vector-DsRed, miR150-DsRed, miR34a-DsRed, miR326-DsRed or miR193a-DsRed. [score:1]
Arc mRNA was significantly increased after treatment with miR-326, but not miR-34a, PNA-AS (Figure 5C). [score:1]
There was also no detectable dendritic staining for miR-326 (Fig. 9B). [score:1]
miR-193a enhanced repression by both miR-34a and miR-326. [score:1]
The seed binding site of miR-193a is close (5 nts) to the first miR-326 site but 360 nts distant from miR-34a. [score:1]
PNA modified antisense oligonucleotides (PNA-AS) complementary to miR-326, miR-34a and miR-19a were purchased from Panagene Inc. [score:1]
More moderate effects were obtained for miR-326. [score:1]
Unstimulated hippocampal neurons were transfected at DIV8 with PNA-AS complementary to miR-34a, miR-326 and miR-193a and cells were harvested 48 hours later for qPCR or western blot. [score:1]
The sensor construct of miR-326 showed the same effect as deleting both miR-326 binding sites. [score:1]
Taken together, the results suggest that under basal (non-stimulated) conditions the levels of miR-34a and miR-326 in distal dendrites is much lower than in the cell body. [score:1]
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2
[+] score: 93
Assessment of normalized expression data for all miRNAs in skin samples obtained from both aGvHD and control rats showed significant differential expression of three miRNAs, with upregulation of miR-34b (2.7-fold change, p = 0.013) and miR-3596d (2.4-fold change, p = 0.006) and downregulation of miR-326 (−2.6-fold change, p = 0.009) in aGvHD samples (Figures 1A,B). [score:11]
Target prediction and pathway analysis identified Notch1 as a possible target in the network of differentially expressed miRNAs and genes in both skin and intestinal T cells, where it is potentially targeted by both miR-21 and miR-326. [score:9]
In particular, downregulation of miR-874 (−2.89-fold change, p = 0.002), mir-20b (−3.37-fold change, p = 0.005), miR-330 (−4.11-fold change, p = 0.006), and miR-326 (−2.22-fold change, p = 0.008), and upregulation of miR-3545-5p (1.97-fold change, p = 0.006), miR-3548 (2.59-fold change, p = 0.006), and miR-21 (3.52-fold change, p = 0.017) was observed. [score:7]
When compared to T cells from peripheral blood, qRT-PCR analyses of purified TCRαβ [+] blood T cells from the same rats indicated a similar expression pattern, with upregulation of miR-21, miR-99a, miR-223, miR-326, and miR-345-5p (Figure 6D), indicating that the GvHD grade during sampling of T cells may be crucial in terms of miRNA expression. [score:7]
Moreover, we found that miR-99a, miR-326, and miR-345-5p, which were all indicated as downregulated by NanoString were detected as upregulated by qRT-PCR (Figure 6C). [score:7]
Here, miR-125a-5p, miR-326, miR-345-5p, and miR-743b were downregulated in both intestinal tissue and intestinal T cells, while miR-17-1-3p, miR-290, and miR-3548 were upregulated (Figure 6E). [score:7]
In addition, we detected upregulation of another predicted target gene for miR-326, the transcription factor Ets1 (Figure 2B). [score:6]
Further validation by qRT-PCR analysis of skin samples obtained from the same and another independent transplantation experiment showed trends toward increased expression of miR-34b and decreased expression of miR-326 (Figure 1C). [score:5]
miR-326 and miR-34b Are Dysregulated in Skin and May Potentially Target Notch1 and Inflammatory Cytokine Genes. [score:4]
This analysis demonstrated that both miR-326 and miR-34b may converge on at least two gene targets, Notch1 and Snai1 (Figure 2A), although these genes were not differentially expressed in skin tissues from aGvHD rats compared to controls (Figure 2B). [score:4]
, which incorporates existing data on genes regulated by miRNAs from the literature, indicated that both miR-34b and miR-326 may share at least two target genes, Notch1 and Snai1 (21– 24). [score:4]
We searched for predicted gene targets for miR-326 and miR-34b using QIAGEN’s IPA software. [score:3]
In gliomas, miR-326 has been shown to participate in a feedback loop with Notch, where miR-326 expression is specifically repressed by Notch (22). [score:3]
We did not detect differential expression of miR-34b or miR-326 in intestinal tissues of rats, and this may reflect the more severe pathology that is observed in skin rather than intestines of rats but also differences in tissue pathology. [score:3]
We also detected differential expression of miR-326 in intestinal and blood T cells but not in intestinal tissues. [score:3]
As we were unable to purify high enough numbers of skin T cells, it is presently unknown whether the differentially expressed miR-326 stems from the infiltrating alloreactive T cells or from other immune or non-immune cells in the skin tissue. [score:3]
miR-326 may additionally regulate the histone deacetylase 3 (Hdac3) gene. [score:2]
In the skin, NanoString analysis indicated differential expression of miR-34b and miR-326 in rats with aGvHD compared to controls, although only a trend was observed by qRT-PCR. [score:2]
The generated network depicted in Figure 7A demonstrates that miR-21, miR-223, and miR-326 may all interact in the same network of molecular responses related to T cell activation and migration. [score:1]
As input for the analysis, we chose miR-21, miR-99a, miR-223, miR-326, miR-345-5p, and miR-743b, and also genes involved in GvHD pathogenesis as well as T cell activation, proliferation, and migration. [score:1]
Also, miR-326 has not previously been implicated in aGvHD in any species. [score:1]
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3
[+] score: 20
In input samples, all three miRNAs examined (miR-34a, miR-19a, miR-326) showed enhanced expression 30 min post-HFS and decreased expression below the contralateral control level when HFS was given in the presence of AP5 (Figure 4A). [score:5]
When AP5 was infused prior to HFS, the Ago2/IP expression ratio of miR-19a and miR-326 was increased, indicating NMDAR -dependent dissociation of these miRNA from Ago2 (Figure 4C). [score:3]
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]
In contrast, miR-19a showed no change and miR-326 had a significantly decreased Ago2/IP expression ratio following HFS. [score:3]
The enhanced expression of miRNA and enhanced associated with Ago2 was specific to NMDA receptor -dependent LTP induction, as was the decrease in the Ago2/input ratio for miR-let7f and miR-326. [score:3]
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4
[+] score: 18
In addition, both miRNA-324-5p targeting gli1 and miRNA-326 regulating the expression of Smo and Gli1 by cooperating with miRNA-324-5p 33 were highly expressed in LX2, but not in CP-MSC (Fig. 5A). [score:8]
It was previously reported that miRNA-125b, miRNA-324-5p and miRNA-326 targeted Hh target genes in human medulloblastoma cell lines 33. [score:5]
The expression of both miRNA-324-5p and miRNA-326 inhibiting gli1 was lower in CP-MSCs than in healthy human liver or LX2 (Fig. 5A). [score:5]
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5
[+] score: 17
Other miRNAs from this paper: rno-mir-330, rno-mir-485, rno-mir-761, rno-mir-666
Target prediction and GO analysis of miR-326-3p/330-5p, miR-485-5p (miR-485-5p/1698/1703/1962), miR-666-3p and miR-761-5p showed enrichment for terms associated with synaptic transmission, plasticity, neurotransmitter synthesis and vesicular release, in both miRNA targets (figure 4 a) and GO terms (figure 4 b and table 3; and the electronic supplementary material, table S2). [score:5]
Many of the miRNAs that were identified are encoded within the introns of host genes that are expressed in hippocampus: miR-326 (Arrb1, β-arrestin), miR-330 (Eml2, echinoderm microtubule associate protein like 2) and miR-761 (Nrd1, Nardilysin) (electronic supplementary material, figure S3). [score:3]
Several of the corresponding miRNAs, including miR-326/miR-330, miR-485, miR-666 and miR-761 were found to be developmentally regulated in the hippocampus. [score:3]
Ingenuity pathway analysis was performed on predicted targets of miR-326-3p/miR-330-5p, miR-485-5p, miR-666-3p and miR-761 using the T argetS can v. 6.2 algorithm [49– 51]. [score:3]
We found that four of the discovered motifs (figure 3 a) in the destabilized gene set corresponded to seed domains of miRNAs miR-326-3p/miR-330-5p, miR-485-5p, miR-666-3p and miR-761. [score:1]
Transcript levels for miR-326-3p, miR-485-5p, miR-666-3p and miR-761 increased by threefold to 12-fold by 14 days post parturition (figure 4 c) (n = 3 animals per time point). [score:1]
11 × 10 [−7] – 1.36 × 10 [−2] axon guidance signalling6.93 × 10 [−4] RAN signalling7.63 × 10 [−4] netrin signalling2.97 × 10 [−3] miR-326/miR-330 top canonical pathways. [score:1]
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6
[+] score: 7
For instance, miR-326 inhibits Notch expression and is also negatively regulated by Notch, establishing a regulatory feedback loop [43]. [score:7]
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7
[+] score: 6
Similarly, some down-regulated miRNAs, such as miR-326 and miR-30c, were also associated with no change in their primary transcripts (Figure 5D and E). [score:4]
Among these miRNAs with shared directions of change in in vitro cultured hippocampal neurons and in vivo hippocampal CA1 regions after either neuronal stimulation or contextual conditioning were miR-24, miR-326, miR-320, miR-21 and miR-10b. [score:2]
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8
[+] score: 5
As shown in Figure 5b, VEGFA were targeted by the greatest number of the differential miRNAs, among which miR-429, miR-200b and miR-200c also interacted with VEGFC; in contrast, VEGFB was targeted only by miR-18a, miR-326, miR-330 and miR-128. [score:5]
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9
[+] score: 2
In cancer cells, miR-326 [17], miR-34a [18], miR-206 [19], let-7 [35] have been shown to regulate the Notch signaling pathway. [score:2]
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10
[+] score: 1
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-21, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, 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-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-98, mmu-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, mmu-mir-133a-2, 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-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-33, rno-mir-98, rno-mir-126a, rno-mir-133a, rno-mir-135a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-203a, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, mmu-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, mmu-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-1, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
Type of site Context+ Context Structure Energy Is experimental validated rno-miR-326-5p MIMAT0017028 3 8mer 7mer-m8 imperfect −0.442 −0.242 431 −65.97 TRUE rno-miR-485-5p MIMAT0003203 2 7mer-m8 −0.343 −0.372 290 −34.96 TRUE rno-miR-300-5p MIMAT0004743 1 8mer −0.338 −0.421 156 −15.16 TRUE rno-miR-702-5p MIMAT0017884 1 8mer −0.317 −0.274 142 −13.86 TRUE rno-miR-203b-3p MIMAT0017800 2 7mer-m8 −0.298 −0.421 295 −29.93 TRUE rno-miR-33-3p MIMAT0017104 2 8mer 7mer-m8 −0.297 −0.813 305 −22.7 TRUE rno-miR-466b-3p MIMAT0017285 1 8mer −0.295 −0.47 159 −15.26 TRUE rno-miR-532-5p MIMAT0005322 1 7mer-m8 −0.268 −0.302 151 −10.71 TRUE rno-miR-511-5p MIMAT0012829 1 7mer-m8 −0.268 −0.302 152 −10.37 TRUE rno-miR-343 MIMAT0000591 1 7mer-m8 −0.262 −0.24 140 −13.75 TRUE rno-miR-203a-3p MIMAT0000876 1 8mer −0.245 −0. [score:1]
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11
[+] score: 1
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-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, 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-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, 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-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
Sharbati-Tehrani et al., [67] have reported 4 new miRNAs (miR-326, miR-423-3p, miR-484 and miR-451,) that could not be identified in our study, which could be attributed to the use of very specialized tissues (Jejunium, spleen, ileum and kidney) for their study. [score:1]
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8 -55.3 -90.4 mmu-miR-34c* -3.7 -1.7 -6.5 mmu-miR-709 -2.9 -2.4 -4.3 mmu-miR-326 -3.9 -2.9 -5.6 rno-miR-664 -1.8 -2.2 -3.6 mmu-miR-350 -1.4 -110.5 -5.1 mmu-let-7e 1.4 -7.6 -5.1 mmu-miR-542–5p -1.9 -5.2 -5.1 rno-miR-20b-5p -3.0 -4.5 -5.0 mmu-miR-374 -1.7 -3.7 -4.4 To understand the cardiovascular benefit of resveratrol in ischaemia/repurfusion, we included longevinex, a commercial formulation of resveratrol by gavage to rat. [score:1]
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The authors also demonstrated that resilient rats differed from vulnerable rats in the set of multiple blood-circulating miRNAs, namely, reduction in miR-139-5p, miR-28-3p, miR-326-3p, and miR-99b-5p in resilient animals and reduction in miR-24-2-5p, miR-27a-3p, miR-30e-5p, miR-3590-3p, miR-362-3p and miR-532-5p levels in vulnerable animals. [score:1]
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Several recent reports have highlighted the post-transcriptional repression of HMGA proteins by non-coding RNAs and, in particular, numerous miRNAs with this activity have been identified (let-7a, miR-15, miR-16, miR-26a, miR-34b, miR-196a2, miR-326, miR-432, miR-548c-3p, miR-570, miR-603) (53, 54). [score:1]
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