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15 publications mentioning rno-mir-708

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-708. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 74
Meanwhile, the expression of miR-17 and miR-708 were analyzed before and after differentiation indicating the downregulation of miR-17 and upregulation of miR-708 upon differentiation of c-kit(+) cells (Figure 2F), suggesting that miR-708 may positively regulate differentiation of cardiac stem/progenitor cells. [score:10]
Enforced expression of miR-708 in CSCs/CPCs was able to decrease the expression of PPARα, N-Ras and Mtss1 as shown in Figure 4C–E, indicating miR-708 mimics were able to interact with target genes in CSCs/CPCs regulating cellular differentiation, although additional works are still required to identify and confirm the target genes through which miR-708 promotes cardiomyocytes differentiation. [score:10]
After 24 h, RNA was isolated and gene expression was analyzed for predicted target genes including PPARα (peroxisome proliferator-activated receptor alpha) which has not been reported yet, and N-Ras (N-Rasproto-oncogene) and Mtss1 (metastasissuppressor 1) which have been reported to be two target genes of miR-708 in rat [20, 21]. [score:9]
In this report, we determined the differentially expressed miRNAs in neonatal hearts compared to adult rat hearts, finding the enrichment of miR-708 in neonatal cardiomyocytes and upregulation of miR-708 upon CSCs/CPCs differentiation. [score:5]
2.2. miR-708 Was Upregulated upon Differentiation of Cardiac Stem/Progenitor Cells. [score:4]
In order to further determine the expression pattern of miR-708 in neonatal cardiomyocytes, c-kit(+) cells were purified from fresh neonatal rat hearts through cell isolation and fluorescence-activated cell sorter (FACS) analysis, and further confirmed by immunofluorescence staining (Figure 1C,D). [score:3]
These findings strengthened the potential of applying miRNAs for regeneration of injured heart, and demonstrated miR-708 as a novel candidate for treatment of heart diseases. [score:3]
miRNA analysis showed a higher expression of miR-708 in c-kit(−) non-progenitor cardiomyocytes than c-kit(+) progenitor cells (Figure 1E). [score:3]
The gene expression analysis indicated the higher levels of cardiomyocyte markers TnnT2 and NKX2.5 after 1 week of differentiation induction in the presence of miR-708 (Figure 3C). [score:3]
In this study, miR-708 was identified to be abundant in the neonatal heart while the expression level markedly reduced in adult rat hearts. [score:3]
The overexpression of miR-708 in the c-kit(+) cells was confirmed by quantitative real-time PCR analysis (Figure 3B). [score:3]
Overexpression, miR-708 was demonstrated to induce differentiation of CSCs/CPCs. [score:3]
Overexpression of miR-708 is able to promote cardiomyocyte differentiation of cardiac stem/progenitor cells. [score:3]
Overexpression of miR-708 promoted differentiation of CSCs to cardiomyocytes. [score:3]
Identification of miR-708 as a Cardiomyocytes-Enriched miRNA in the Heart of Neonatal Rats. [score:1]
In order to determine the function of miR-708 during cell differentiation, the c-kit(+) cells were transfected with miR-708 or control, and cultured for ~3 weeks under the differentiation condition (Figures 2A and 3A). [score:1]
As shown in Figure 1A, a subset of neonatal hearts-enriched miRNAs including miR-708 were identified (Figure 1A). [score:1]
As shown in Figure 4A,B, rat PPARα mRNA has one binding site to miR-708, which is highly conserved between species. [score:1]
miR-708 transfected cells had more capability to differentiate to cardiomyocytes and form the strips of heart muscle (Figure 3A). [score:1]
The miRNA mimic sequences for miR-708: 5′-AAGGAGCUUACAAUCUAGCUGGG-3′. [score:1]
miR-708 is enriched in the neonatal cardiomyocytes of rats. [score:1]
In order to confirm the exogenous miR-708 is functional in cells, c-kit(+) CSCs/CPCs were transfected with miR-708 mimics. [score:1]
2.3. miR-708 Promoted Differentiation of Cardiac Stem/Progenitor Cells into Cardiomyocytes. [score:1]
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2
[+] score: 69
Other miRNAs from this paper: rno-mir-499
The results of the present miRNA and target gene analyses suggest that the brain-expressed miRNAs miR-499, miR-708 and miR-1908 may contribute to the development of BD. [score:6]
The target gene enrichment analysis showed no significant enrichment of BD -associated genes within the targets of miR-499, miR-708 or miR-1908 (Table 2). [score:5]
The subsequent analyses were restricted to brain-expressed target genes of miR-499, miR-708 and miR-1908, with a gene -based association P-value of <0.05. [score:5]
After Bonferroni correction, miR-1908 had one (KLC2) and miR-708 had two significant target genes (NRAS and CREB1), whereas miR-499 had four significant target genes (GPC6, C16orf72, WDR82 and CACNB2). [score:5]
[35] The regional association plots and the miRNA expression data in human brain tissue suggest that the three brain-expressed miRNAs, that is, miR-499, miR-708 and miR-1908, are the most promising candidates for further analyses. [score:5]
[60] Our target gene analysis revealed that miR-708 had two significant target genes. [score:5]
Regional association plots and expression data suggest that the miRNAs miR-499, miR-708 and miR-1908 are the most promising candidates in terms of the development of BD. [score:4]
Another recent study found that miR-708 regulated the expression of neuronatin, which is a membrane protein in the endoplasmic reticulum. [score:4]
Three of these (miR-499, miR-708 and miR-135a-1) were also found to be expressed in the rat forebrain. [score:3]
[58] In another study, Xu et al. [59] demonstrated an altered expression profile for miR-708 in mouse hippocampal neurons and showed that this was mediated by oxidative stress. [score:3]
Eight of the nine associated miRNAs were located in a host gene, including the three brain-expressed miRNAs miR-499, miR-708 and miR-1908. [score:3]
Target gene and pathway analysis for miR-499, miR-708 and miR-1908. [score:3]
As expected, transfection of the non-effective miR-708 expression construct had no significant effect on spine morphological parameters. [score:3]
Alternative strategies for miR-708 expression, together with miR-499/708 loss-of-function approaches, must be tested before definite conclusions regarding the role of these miRNAs in dendritic spine morphogenesis can be drawn. [score:3]
To test the possible involvement of miR-499 or miR-708 in the regulation of synaptic function, experiments were performed to investigate the effect of miR-499 and miR-708 overexpression on dendritic spine morphogenesis in primary rat hippocampal neurons. [score:2]
[3] A recent study of postpartum psychosis—a disorder that often heralds the incipient onset of BD [57]—suggested differential expression of miR-708 in the monocytes of affected patients compared with controls. [score:2]
The target genes that drive a particular pathway are listed in Supplementary Table 3. Luciferase assays revealed efficient processing of pri-miR-499, but not pri-miR-708, upon transfection of the respective constructs in neurons (Supplementary Figure 6). [score:2]
However, only the results for miR-499 can be considered robust, as the miR-708 expression construct did not increase miR-708 in primary neurons effectively. [score:2]
Functional analyses of miR-499 and miR-708 in rat hippocampal neurons. [score:1]
The results of the functional analyses of miR-499 and miR-708 in rat hippocampal neurons revealed no major contribution of these miRNAs to the morphogenesis of dendritic spines, which represent the major sites of synaptic contact. [score:1]
The miRNA miR-708 is located in the first intron of ODZ4 (odd Oz/ten-m homolog 4, TENM4), which has been reported as a genome-wide significant susceptibility gene for BD. [score:1]
To investigate the potential involvement of miR-499-5p and miR-708-5p in dendritic spine morphogenesis, hippocampal neurons of embryonic day-18 Sprague–Dawley rats (Charles River Laboratories, Sulzfeld, Germany) were transfected with miRNA -overexpressing constructs for 6 days before fixation. [score:1]
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3
[+] score: 57
Since miRNAs typically alter the gene expression in mammals through translational inhibition, it is likely that miR-708 negatively regulates the MAPK pathway genes. [score:8]
Accordingly, our data revealed that MPS downregulates miR-708, which potentially regulates the expression of genes involved in neurotrophin signaling, MAP kinase signaling and axon guidance pathway (Lewis et al., 2005; Xu et al., 2012; Vitucci et al., 2016). [score:7]
It can be further inferred that downregulation of miR-708 and upregulation of Rasd2 and Mapk10 genes by PS found in our work could contribute to the promotion of neuronal proliferation, likely contributing to the neuronal protection and increased resilience in association With MPS. [score:7]
Our present data indicate that indeed miR-708 may downregulate Mapk10 and Rasd2 expression. [score:6]
Rno-miR-708-3p potentially targets the Map3k13, Mapk10, Kras, Rap1b, Nras, Rasd2 and Csf1 mRNAs to potentially regulate neuron development and cell proliferation (Figure 5C). [score:5]
Moreover, upregulation of miR-708 is associated with increased oxidative stress and subsequent neurodegenerative processes (Bishop et al., 2010). [score:4]
miR-708 was shown to be upregulated in hippocampal neurons in response to oxidative stress (Xu et al., 2012). [score:4]
Although experimental confirmation at large is still lacking, our study confirmed that miR-708 arguably is a regulator of Mapk10 and Rasd2 expression. [score:4]
This result is consistent with our study demonstrating lower expression of miR-708 in the MPS animals that were also more resilient to stress. [score:3]
MAPK signaling pathway genes, namely Map3k13, Mapk10, Kras, Rap1b, Nras, Rasd2 and Csf1 were predicted bioinformatically to be among main targets of miR-708. [score:3]
Notably, recent work studying biomarkers of resilience or vulnerability to stress in rats demonstrated that the expression of miR-708-5p along with miR-126a-3p was higher at the medial prefrontal cortex (mPFC) of vulnerable rats (Chen et al., 2015). [score:3]
Compared to non-stressed rats, rno-miR-708-3p was significantly downregulated in the PFC of stressed animals (p < 0.05, n = 3; Figure 5A). [score:3]
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4
[+] score: 53
Interestingly, miR-22, miR-1224 and miR-125-3p were initially up-regulated under EGF and bFGF treatment, but reversed their quantitative expression in the presence of IGF-1. In addition, miR-214 and miR-708 were expressed inconsistently in Group A while their expression went down in Group B. To validate the microRNA microarray expression data, a qRT-PCR assay was conducted to confirm the expression levels of three randomly selected microRNAs (let 7-b, miR-181a, and miR26a). [score:13]
Since the down-regulation of microRNAs may cause the up-regulation of targeted genes, we hypothesized that the presence of IGF-1 triggers the expression of certain genes by down -regulating key microRNAs (miR-1224, miR-125a-3p, miR-214, miR-22, miR-320, miR-708, and miR-93), which in turn enhance NPCs proliferation and survivability. [score:12]
However, BMSC-derived NPCs with addition of IGF-1 showed 12 microRNAs which include miR-22, miR-1224, miR-125a-3p, miR-214, miR-320, miR-708 and miR-93 were consistently down-regulated and only miR-496 remained up-regulated compared to Group C from Day 1 to Day 5. The let-7 family (let-7b, let-7c, let-7d, let-7e and let-7i) were constantly down-regulated in both groups. [score:9]
Furthermore, the introduction of IGF-1 triggers the down-regulation of several microRNAs (miR-214, miR-22, miR-320 and miR-708) with their inconsistent differential expression in Group A. The inhibition of miR-214 has been reported to decrease the level of apoptosis in HeLa cells [34]. [score:8]
The down-regulation of miR-708 was reported to be involved in the enhancement of cell proliferation [36] and the expression of miR-708 has been reported to be associated with PI3K/Akt signaling pathways [37]. [score:6]
Dileepan M. Jude J. A. Rao S. P. Walseth T. F. Panettieri R. A. Subramanian S. Kannan M. S. MicroRNA-708 regulates CD38 expression through signaling pathways JNK MAP kinase and PTEN/AKT in human airway smooth muscle cells Respir. [score:3]
MiR-1224, miR-708 and miR-93 were excluded from analysis since there is no mRNA associated with negative regulation of apoptosis. [score:2]
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5
[+] score: 41
In the 1 h incubation (Fig. 3), with the exception of rno-miR-142-3p and rno-miR-335, the relative expression levels of the miRNAs at 2.8G were similar to those of freshly isolated islets (Fig. 3; p<0.05 vs 2.8G in Wistar), i. e. GK miRNAs significantly -upregulated in the microarrays consistently exhibited higher levels of expression than the Wistar miRNAs, whereas rno-miR-708 which was found to be downregulated in GK was minimally expressed. [score:13]
Rat miR-375, miR-132 and miR-708 are indicated for reference, representing no significant change (dark tones), upregulated (yellow tones) and downregulated (blue tones) miRNAs in GK. [score:7]
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]
We also included the most consistently down-regulated miRNA, rno-miR-708, in the GK rat islets for validation. [score:4]
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]
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6
[+] score: 8
Among the miRNAs, miR-214, miR-199a-5p, miR-150, miR-199a-3p, miR-351, miR-145, miR-764, miR-497 and miR-92b were upregulated, whilst miR-7a, miR-325-5p, miR-485, miR-708, miR-344-3p, let-7f, miR-26b, miR-129, miR-29c and let-7a were downregulated. [score:7]
These miRNAs include miR-214, miR-199a-5p, miR-150, miR-351, miR-145, miR-92b, miR-7a, miR-485, miR-708, let-7f, miR-26b, miR-129, miR-29c and let-7a. [score:1]
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7
[+] score: 4
Pregnant rats fed the PO diet during the first 12 days of pregnancy showed significantly higher expression of adipose miR-668 and miR-674–5p and lower expression of miR-708 compared with rats fed the SO, OO, FO, and LO diets. [score:4]
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8
[+] score: 3
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]
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9
[+] score: 3
Compared to the other 2 groups, 21 miRNAs are upregulated in 6-hour group as shown in the upper portion of Fig. 2, miR-9, miR-204, miR-335, miR-23a, miR-708, miR-146a, miR-325-5p, miR-106b, miR-143, miR-140, miR-376b-3p, miR-7a, miR-541, miR-185, miR-499, miR-127*, miR-320, miR-140*, miR-145*, miR-423*, miR-378. [score:3]
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10
[+] 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-222, 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, 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
E [2] decreased miR-146a, miR 125a, miR-125b, let-7e, miR-126, miR-145, and miR-143 and increased miR-223, miR-451, miR-486, miR-148a, miR-18a, and miR-708 expression in mouse splenic lymphocytes [199]. [score:3]
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11
[+] score: 2
Twelve miRNAs (miR-135a, miR-190, miR-22, miR-347, miR-376*, miR-380*, miR-382, miR-383, miR-702-3p, miR-708, miR-873, and miR-99b*) were regulated only in CCE rats (p < 0.05 vs. [score:2]
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12
[+] score: 2
Recent studies have successfully established a functional link between cell survival and a discrete group of survival -regulating miRNAs, including miRNA-1 [14], miRNA-125 [15], miRNA-206 [14], miRNA-210 [16, 17] and miRNA-708 [18]. [score:2]
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13
[+] score: 2
qPCR analysis revealed that lnc-PCF was significantly enriched in miR-344a-5p as compared with that in non -targeting miR-708-3p (Figure 4d). [score:2]
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14
[+] score: 2
Additionally, 34 miRNAs were significantly deregulated due to sham laparotomy but were unaffected following PH (e. g., rno-miR-205, rno-miR-295, rno-miR-337 and rno-miR-708). [score:2]
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15
[+] score: 1
Other miRNAs from this paper: rno-mir-21, rno-mir-30a, rno-mir-34a
Metformin induces ER stress -dependent apoptosis through miR-708-5p/NNAT pathway in prostate cancer [28]. [score:1]
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