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28 publications mentioning rno-mir-10b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-10b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 149
Other miRNAs from this paper: mmu-mir-10b, hsa-mir-10a, hsa-mir-10b, mmu-mir-10a, rno-mir-10a
Hierarchical clustering of the differentiated expressed genes (DEGs) showed that the DEG expression patterns were quite similar regardless of whether miR-10a or miR-10b was overexpressed in GCs, implying similar functions for miR-10a and miR-10b in GCs (Fig. 4B). [score:7]
To determine whether BDNF was direct target of miR-10a and miR-10b, the putative miR-10 target 3′ UTR was cloned into a reporter plasmid downstream of a luciferase gene (Fig. 5F). [score:6]
To summarize, these results showed that FSH, FGF9 and TGF pathway signalling could inhibit miR-10a and miR-10b expression in hGCs, mGCs and rGCs, which suggests that the FSH/FGF9 and TGF-β pathway may function as an upstream regulator of miR-10a and miR-10b in GCs; these effects were conserved among different species (Fig. 3D). [score:6]
Similar to GCs overexpressing the miR-10 family, proliferation was inhibited (Fig. 6A) and apoptosis was induced (Fig. 6B) upon BDNF knockdown. [score:6]
To further identify the associated pathways and direct targets of miR-10a and miR-10b in GCs, RNA-seq was performed for miR-10a/b -overexpressing granulosa cells (Fig. 4A). [score:6]
In conclusion, we found that miR-10 family members, including miR-10a and miR-10b, are expressed at basal levels in GCs but are highly expressed in theca and stroma cells within the ovary. [score:5]
miR-10a and miR-10b directly targeted BDNF in GCs, suggesting that the miR-10 family might also affect other normal ovary functions apart from GC development. [score:5]
Here, we demonstrated that two members in the miR-10 family, miR-10a and miR-10b, function as anti-proliferation and pro-apoptosis factors in human, mouse and rat GCs by directly targeting the 3′ UTR of BDNF in GCs. [score:4]
Gene ontology results suggested that miR-10a and miR-10b target genes were highly related to cell growth, proliferation, development and reproduction (Fig. 4C and Supplementary Fig. 1D). [score:4]
miR-10a and miR-10b expression in granulosa cells is regulated by extrinsic/intrinsic signals. [score:4]
BDNF is a direct target of the miR-10 family in granulosa cells. [score:4]
To prove that the downstream target of the miR-10 family, BDNF, could mediate the function of the miR-10 family in GCs, shRNA was used to knockdown BDNF in GCs (Supplementary Fig. 1G). [score:4]
These results indicated that BDNF was a direct target of miR-10a and miR-10b in GCs. [score:4]
Using fluorescence in situ hybridization (FISH), both miR-10a and miR-10b were shown to be expressed in mouse and rat GCs (Fig. 1C and Supplementary Fig. 1C). [score:3]
miR-10 family expression in normal and atretic granulosa cells. [score:3]
miR-10 family expression was abundant in the remaining GCs in atretic follicles (Fig. 1F). [score:3]
A putative miR-10 binding site in the BDNF 3′-untranslated region (UTR) was also identified (Fig. 5B). [score:3]
By using RNA-seq and qPCR, miR-10a and miR-10b were shown to inhibit many key genes within the TGF-β pathway, including ligands, receptors and transcription factors. [score:3]
To further confirm that the anti-proliferative and pro-apoptotic functions of the miR-10 family in GCs are at least partially via BDNF, recombinant BDNF was used to treat miR-10a/b -overexpressing GCs. [score:3]
By using RNA-seq screening, bioinformatics prediction, qPCR, Western blot analysis, luciferase reporter assays and FISH-IF validation, BDNF was identified as a direct target of the miR-10 family in GCs. [score:3]
As validated by, BDNF was inhibited at the mRNA by the miR-10 family in GCs (Fig. 5D). [score:3]
The opposite expression patterns for BDNF and the miR-10 family in GCs further indicated the repressive effect of miR-10a/b on BDNF (Fig. 5C). [score:3]
MiRNAs are small non-coding RNAs that repress mRNA translation at the post-transcriptional level 7. Many miRNAs that share a common “seed sequence” form a family and are located on different chromosomes in the genome; one such example is the miR-10 family, which is a highly conserved family among different species. [score:3]
As shown in Fig. 3B, treatment with these TGF-β superfamily ligands inhibited miR-10a and miR-10b in GCs. [score:3]
In this study, we found that these critical regulatory factors could repress miR-10a and miR-10b in granulosa cells, further indicating the negative roles of the miR-10 family during folliculogenesis. [score:2]
Both miR-10a and miR-10b could repress proliferation and induce apoptosis in human, mouse and rat granulosa cells, at least partly through repressing BDNF by directly binding to its 3′ UTR. [score:2]
Taken together, these results suggest that miR-10a and miR-10b might play a negative role in follicle development. [score:2]
How to cite this article: Jiajie, T. et al. Conserved miR-10 family represses proliferation and induces apoptosis in ovarian granulosa cells. [score:1]
However, the function of the miR-10 family is still unknown in other species, such as humans, mice and rats. [score:1]
The general function of the miR-10 family in granulosa cells. [score:1]
As expected, BDNF could rescue GC apoptosis caused by miR-10a and miR-10b mimic transfection (Fig. 6D). [score:1]
miR-10 family members repressed proliferation and induced apoptosis in granulosa cells. [score:1]
miR-10a and miR-10b mimic treatment significantly reduced the viability of human, mouse and rat GCs (Fig. 2A). [score:1]
The miR-10 family has two members, miR-10a and miR-10b. [score:1]
In contrast, apoptosis was induced by miR-10a and miR-10b in GCs of different species (Fig. 2C). [score:1]
Taken together, the results showed that BDNF could at least partially mediate the function of the miR-10 family in GCs. [score:1]
Some essential genes in this pathway, including ACVR2A, ACVR2B, SMAD1, SMAD3, BMP4 and AMH, were significantly repressed by both miR-10a and miR-10b in GCs (Fig. 4E). [score:1]
We also identified six asymmetric bulges in the structures of the hsa-miR-10a and hsa-miR-10b duplexes (Fig. 1B). [score:1]
BDNF rescues miR-10 family-caused effects in GCs. [score:1]
BDNF rescues miR-10a- and miR-10b -induced proliferation repression and apoptosis induction in GCs. [score:1]
It was also reported that miR-10 could repress proliferation in porcine granulosa cells 19. [score:1]
These data confirmed that the miR-10 family simultaneously represses proliferation and induces apoptosis in GCs; this effect is conserved among humans, mice and rats. [score:1]
HEK293T cells grown in 24-well plates were transfected with 50 nM miR-10a and miR-10b mimic (GenePharma, China) and 100 ng of pmirGLO vector (Promega, USA) tagged with either a BDNF 3′ UTR that includes the miR-10 binding sites or the empty plasmid using Lipofectamine 2000 (Invitrogen, USA). [score:1]
The nucleotide sequence of the miR-10a and miR-10b precursors are highly conserved in mammals (Fig. 1A). [score:1]
Both miR-10a and miR-10b gradually decreased during follicle maturation (Fig. 1D) and increased by follicle atresia, as determined by (Fig. 1E). [score:1]
BMP4 and BMP15 are from the BMP family, and Activin A is a member of the Activin family, and all are components of the TGF-β pathway 23, suggesting that the TGF-β signalling pathway might also repress the miR-10 family in GCs. [score:1]
Moreover, the miR-10 family and the TGF-β pathway form a negative feedback loop in GCs. [score:1]
This study provides new insights into how the miR-10 family functions in the female reproductive system. [score:1]
These results indicate that the miR-10 family has similar functions in GCs in different species. [score:1]
miRCURY LNA miRNA detection probes for miR-10a and miR-10b were purchased from Exiqon (613307–310 and 613028–310, respectively; Vedbaek, Denmark). [score:1]
The seed region (UCAAGUA) of miR-10 is conserved among vertebrate species. [score:1]
As expected, the mediator of FSH in GCs, cAMP, also greatly repressed miR-10a and miR-10b in GCs (Fig. 3A). [score:1]
miR-10 family is highly conserved among different species. [score:1]
Consistent with these observations, our data showed that the miR-10 family decreased proliferation and induced apoptosis in granulosa cell. [score:1]
Identification of miR-10a and miR-10b in granulosa cells. [score:1]
By using Ki-67 staining, the proliferation of GCs was also found to be repressed by the miR-10 family (Fig. 2B). [score:1]
Effects of exposure to hormone and growth factors on miR-10a and miR-10b in granulosa cells. [score:1]
The effect of the miR-10 family on GCs on a transcriptome-wide scale. [score:1]
miR-10 was identified as a specific marker for mouse granulosa cells from previous miRNA-sequencing results 17. [score:1]
The results showed that FGF9 could also greatly repress the miR-10 family in GCs (Fig. 3A). [score:1]
The mature hsa-miR-10a-5p and hsa-miR-10b-5p sequences are UACCCUGUAGAUCCGAAUUUGUG and UACCCUGUAGAACCGAAUUUGUG, respectively, and have only one different nucleotide. [score:1]
To further explore whether BDNF mediates the function of the miR-10 family in GC apoptosis, GCs were co -treated with miR-10 family mimics in the presence of recombinant BDNF or vehicle control. [score:1]
All of the cells were transfected with 20 nM of either miR-10a or miR-10b mimic (GenePharma) using the Lipofectamine RNAiMAX transfection reagent and Opti-MEM medium (Life Technologies) according to the manufacturer’s instructions. [score:1]
Additionally, many hormones and growth factors in the ovary repressed the miR-10 family in GCs. [score:1]
These results indicate that the miR-10a and miR-10b precursors and mature sequences are highly conserved and might have similar functions in mammals. [score:1]
Follicle-stimulating hormone (FSH) could stimulate granulosa cells to convert androgens to oestradiol via aromatase 20 and maintain GC proliferation and maturation 21. miR-10a and miR-10b were significantly decreased by recombinant human FSH in hGCs, mGCs and rGCs (Fig. 3A). [score:1]
These results indicate that autocrine and/or endocrine signals from hormones or growth factors during granulosa cell differentiation are involved in repressing the miR-10 family in GCs. [score:1]
The results showed that both the miR-10a and miR-10b mimics repressed the fluorescence from the 3′ UTR compared with the negative control, indicating that miR-10a and miR-10b could directly bind to the BDNF 3′ UTR. [score:1]
Considering that TGF-β superfamily ligands could greatly repress the miR-10 family in GCs, this result suggests that the miR-10 family and the TGF-β pathway might be involved in a negative feedback loop. [score:1]
miR-10a and miR-10b repress proliferation and induce apoptosis in human, mouse and rat granulosa cells. [score:1]
Based on small RNA-seq from a previous study, miR-10 is a specific marker for mouse granulosa cells 17. [score:1]
Both miR-10a and miR-10b were induced by TGF-β1 in GC. [score:1]
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[+] score: 44
In glioma cells, miR-10b regulates the expression of mRNA for RhoC and urokinase-type plasminogen activator receptor (uPAR) via inhibition of translation of the mRNA encoding homeobox D 10 (HOXD 10), resulting in invasion and metastasis of glioma cells. [score:8]
By performing real-time PCR, Sasayama et al. [29] found that miR-10b expression was upregulated in gliomas and that the expression of miR-10b was associated with higher-grade glioma. [score:8]
In detail, five miRNAs were significantly up-regulated (miR-21, miR-34c-3p, miR-470*, miR-10b, let-7i*) and two miRNAs significantly down-regulated in SP of HCC cells (miR-200a*, miR-148b*). [score:7]
For example, the precursor sequences of the up-regulated miRNAs (miR-21, miR-10b) and down-regulated miR-148b* observed in our study are located at 17q23, 3q23 and 12q13. [score:7]
Similarly, overexpression of miR-10b was also detected in metastatic breast cancer by Ma et al. [30], who showed that increased expression of miR-10b promoted cell migration and invasion. [score:5]
These target genes were PTEN (miR-21), P53 (miR-34c), Rho C (miR-10b), RAS (let-7i), and ZEB1 (miR-200a). [score:3]
As shown in Figure 4A, the results showed that the expression levels of miR-21, miR-34c-3p, miR-16, miR-10b, and let-7i* in SP of HCC cells compared to SP of fetal liver cells were increased 3.5 ± 0.84, 2.1 ± 0.52, 2.2 ± 0.46, 3.9 ± 0.61, and 2.8 ± 0.25 -fold respectively, which were consistent with miRNA microarray results (P < 0.05). [score:2]
Here we validated significant overexpression of miR-10b, miR-21, and miR-34c-3p in SP fractions of HCC compared to SP fractions of normal fetal liver cells. [score:2]
A total of 68 miRNAs, including miR-10b, miR-21, miR-470*, miR-34c-3p, and let-7i*, were identified as overexpressed in SP of HCC cells compared to fetal liver cells. [score:2]
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[+] score: 28
Cluster analysis of over-expressed miRNAs (Figure S1A) and under-expressed miRNAs (Figure S1B) indicated that some deregulated miRNAs might play their roles in groups, such as up-regulated miR-10b and miR-21 and down-regulated miR-200a* and miR-148b*. [score:12]
Most importantly, miR-10b, the second most over-expressed miRNA in SP-HCCs, has been found to be highly expressed in metastatic breast cancer cells and has been shown to positively regulate cell migration and invasion [53]. [score:6]
MiR-10b inhibits the synthesis of the HOXD10 protein and permits the expression of the pro-metastatic gene product RHOC, which in turn favors cancer cell migration and invasion [53]. [score:4]
In this study, miR-10b, miR-21 and miR-92b were frequently over-expressed. [score:3]
Gastroenterology 138 S-116 63 Moriarty CH Pursell B Mercurio AM 2010 miR-10b targets Tiam1: implications for Rac activation and carcinoma migration. [score:3]
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[+] score: 23
Of 148 target sites in 85 genes predicted for rno-miR-10a-5p by DIANA-microT v3.0, 147 are also predicted for the most frequent miR-10b isomiR, reflecting the dominance of the seed region in target recognition. [score:5]
DIANA-microT v3.0 predicts 147 targets in 85 genes for the most abundant rno-miR-10b isomiR (Fig. S2). [score:3]
05) transmural expression gradients for miR-10b, miR-21, miR-99b and miR-486 (Fig. 10). [score:3]
Figure S2 Expression profile of rno-miR-10b isomiRs in mid-myocardium. [score:3]
In comparison, only one of the 10 predicted target genes found for canonical rno-miR-10b is shared with the isomiR. [score:3]
We have found that most miRNAs are not expressed in a gradient across the ventricular wall, with the exceptions of miR-10b, miR-21, miR-99b and miR-486. [score:3]
Surprisingly, miR-10b exhibited no exact mature sequences (see Table S3B); on closer analysis sequences aligned to miR-10b were found to exhibit shifting in the mature miRNA cleavage position with 12.38±0.77% of the reads including 1 extra nt and 87.39±0.91% 2 extra nts from the pre-miR sequence at the 5′ end (see Fig. S2). [score:1]
Deep sequencing shows a transmural gradient (epicardium>endocardium) for miR-10b (Table 2, “grouped on mature”). [score:1]
As discussed above, this group includes no canonical miR-10b, with only 5.6% of reads having the canonical 3′ end (4 [th] and 6 [th] in the list in Fig. S2). [score:1]
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[+] score: 17
The majority of these progression -associated miRNAs, including miR-10a, miR10b, miR-124, miR-125b, miR-126, miR-145, were increasingly downregulated with increasing lesion severity, while 2 miRNAs, miR-21 and miR-200a, were upregulated with advancing tumor progression. [score:7]
Several of the progression -associated miRNAs identified mirror those found to be changed during progression in human normal, DCIS, and IDC breast cancer samples, including an upregulation of miR-21 and a downregulation of miR-10b, miR-125b, and miR-126 [15]. [score:7]
The 8 miRNAs we found from our profiling (specifically, miR-10a, miR-10b, miR-21, miR-124, miR-125b, miR-126, miR-145, and miR-200a) each showed progressive changes in expression with advancing lesion grade. [score:3]
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[+] score: 15
Reduced expression of miR-192, miR-215 and miR-10b in liver samples of rat from fish oil group (Fig. 3B) resulted in a de-repression of their targets plasminogen activator inhibitor type 1 (Serpine1) and insulin-like grow factor 2 (Igf2), as both genes have predicted binding sites for these three miRNAs. [score:7]
Igf2 and Serpine1 are targets of miR-192/215 and miR-10b family. [score:3]
Compared to all other treatments, miR-215 expression was significantly induced by FO consumption, while miR-10b and miR-9a were induced by LO (Fig. 3A). [score:2]
Lower expressions of miR-10b-5p and miR-377–3p were also observed in adult pups of rats fed FO diet compared with SO, OO, and PO diets. [score:2]
Likewise, we observed a decrease in the expression of several hepatic miRNAs, namely miR-192–5p, miR-10b-5p, miR-377–3p, and miR-215 after FO compared with OO and PO diets and miR-21–5p and mir-26b-5p after FO compared with PO diets. [score:1]
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[+] score: 12
Similarly, the expression of oncogenic miRNAs like miR-21, miR-10b, let-7i, miR-34c, were increased more than 2 fold in EpCAM [+] liver cancer cells; whereas miR-125b, miR-200a, miR-148b were most down-regulated. [score:6]
miR-21, miR-10b and miR-34c have been reported to be upregulated in various types of cancers, including HCC [25]. [score:4]
Our previous report also revealed that the relative expression levels of miR-92b, miR-21, miR-34c, miR-10b, and let-7i in EpCAM [+] liver cancer cells compared to fetal liver cells were increased (P<0.05). [score:2]
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[+] score: 11
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-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, 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-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, 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-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
For example, in mouse [14], miR-10b is highly expressed in spinal cord; miR-124 is wi dely expressed in brain tissues; miR-200b, miR-128a, miR-128b, miR-429 are specifically expressed in olfactory bulb; miR-200a is highly expressed in olfactory bulb; miR-7b is highly expressed in hypothalamus. [score:11]
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[+] score: 10
MiR-10 indirectly down-regulates VEGF -mediated angiogenesis in HUVECs by targeting fms-related tyrosine kinase 1 (FLT1), a cell-surface protein that sequesters VEGF [16]. [score:6]
Recent studies also indicate that a panel of miRNAs (i. e., miR-10, miR-15b, miR-16, miR-20a, miR-20b, miR-27a, miR-126, miR-145, miR-195, miR-205, and miR-210) is involved in the regulation of VEGF expression in ECs and tumor cells [16]– [26]. [score:4]
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[+] score: 9
Among them, 12 miRNAs (rno-miR-10b-5p, rno-miR-122-5p, rno-miR-184, rno-miR-1843-5p, rno-miR-196c-5p, rno-miR-199a-5p, rno-miR-202-5p, rno-miR-206-3p, rno-miR-208b-5p, rno-miR-224-5p, rno-miR-298-5p and rno-miR-31a-5p) were significantly upregulated(p<0.01, fold-change >1) compared to the control group and only rno-miR-208a-3p were significantly downregulated (p<0.01, fold-change <-1) (Fig 3). [score:6]
Meanwhile, rno-miR-10b-5p, rno-miR-184, rno-miR-1843-5p, rno-miR-196c-5p, rno-miR-202-5p, rno-miR-206-3p, rno-miR-224-5p, rno-miR-298-5p and rno-miR-31a-5p were reported for the first time to be differentially expressed in HF tissue. [score:3]
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[+] score: 8
Other miRNAs from this paper: rno-mir-19b-1, rno-mir-19b-2
Three protein coding mRNAs and 1 microRNA were down-regulated with statistical significance in GCs following HFD consumption; collagen3a1, gelsolin and decorin (Fig. 2E) and miRNA rno-mir-10b (Fig. 3E). [score:4]
The miRNA rno-mir-10b is highly expressed and demonstrates a modest difference between HFD and CD groups. [score:3]
Expression was determined using the primers and universal probes (Roche, UK) in Supplementary Table 4. For miRNA, the ABI TaqMan miRNA assay for rno-mir-10b was used according to manufacturer’s instructions; snoRNA-U6 was used as control. [score:1]
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[+] score: 8
The mir-196 family regulates Hox8 and Hox7 genes, the function of mir10 is unknown. [score:2]
A few microRNAs are apparently linked to protein coding genes, most notably mir-10 and mir-196 which are located in the (short) intergenic regions in the Hox gene clusters of vertebrates [4- 7]. [score:1]
The mir10 and the mir196 precursors are located at specific positions in the Hox gene clusters [4- 7]. [score:1]
mir10 is a good example of this typical substitution pattern, which gives rise to a hairpin structure. [score:1]
The mir-10b CNB shows the typical pattern of substitutions in a microRNA precursor hairpin: There are two well-conserved arms, of which the mature microRNA is almost absolutely conserved, and a much more variable loop region. [score:1]
Nevertheless, it is conserved across all vertebrate species as shown in Figure 5. Figure 4Alignment and predicted RNA structure of mir-10b. [score:1]
Nevertheless, it is conserved across all vertebrate species as shown in Figure 5. Figure 4Alignment and predicted RNA structure of mir-10b. [score:1]
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[+] score: 8
Among them, miR-27a-3p, let-7a-5p, miR-10b-5p, and miR-23b-3p have been shown to function as regulators of spinal cord development and remo deling, and have been implicated in diseases of the spinal cord [20, 21]. [score:5]
Nine of the miRs (miR-200b-3p, miR-27a-3p, let-7a-5p, miR-21-5p, miR-10b-5p, miR-23b-3p, miR-221-3p, miR-100-5p, and miR-28-5p) were differently expressed at both 24 and 72 hours after reperfusion. [score:3]
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[+] score: 7
miR-448, let-7b, miR-540, miR-296, miR-880, miR-200a, miR-500, miR-10b, miR-336, miR-30d, miR-208, let-7e, miR-142-5p, miR-874, miR-375, miR-879, miR-501, and miR-188 were upregulated, while miR-301b, miR-134, and miR-652 were downregulated in TMH group (Table 5). [score:7]
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[+] score: 6
Inhibition of mib1 and Notch signaling partially rescued the angiogenic defects in miR-10 morphants, suggesting that angiogenic defects in miR-10a/10b morphants are caused by upregulation of Notch signaling (Safdar et al., 2016). [score:6]
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[+] score: 5
Among the down-regulated miRNAs, miR-10b contributes to retinoic acid -induced differentiation of neuroblastoma cells and fatty acid metabolism in liver [26, 27]. [score:4]
9 -45.6 mmu-miR-27b -1.8 -71.4 -462.7 mmu-miR-214* -2.6 -5.0 -43.5 mmu-let-7c-1* -73.2 -204.4 -334.1 mmu-miR-34c -9.4 -26.1 -42.7 mmu-miR-542–3p -5.9 -195.6 -319.8 mmu-miR-706 -9.3 -5.0 -38.7 mmu-miR-487b -2.0 -161.5 -263.9 mmu-miR-467b* -10.1 -2.2 -33.6 rno-miR-17–3p -1.6 -152.0 -248.5 mmu-miR-323–3p -3.7 -23.3 -29.8 mmu-miR-10b -2. 4 -136.6 -223.3 mmu-miR-202–3p -6.5 -5.9 -21.4 mmu-miR-29b -3.0 -135.1 -220.9 mmu-miR-339–5p -1.6 -9.6 -19.6 mmu-miR-297a* -2.4 -128.4 -209.8 mmu-miR-181c -2.0 -10.5 -14.6 mmu-miR-692 -41.5 -115.8 -189.2 mmu-miR-203 -4.6 -6.4 -13.8 mmu-miR-208 -40.6 -113.5 -185.5 mmu-miR-467a* -2.6 -3.9 -11.4 mmu-miR-467c -38.9 -108.6 -177. [score:1]
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[+] score: 5
Finally, there were no changes in expression of mir10a and mir10b, which are known to regulate hoxd10 [39], a gene belonging to the homeobox family, which is key to a number of developmental processes [40] (Fig. 3d). [score:5]
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[+] score: 4
In the chronic liver injury mo dels including the HFD, MCDD, and CCl [4] groups, we found that 3 miRNAs (miR-10b*, miR-410, miR-499) were commonly down-regulated, but were not affected in the acute liver injury mo dels (Fig. 4), suggesting that these miRNAs might serve as biomarkers of steatosis. [score:4]
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[+] score: 4
Moreover, decreased miR-155 and increased miR-27a in the disc may be associated with apoptosis [14, 15], whereas up-regulation of miR-10b and miR-21 is linked to NP cell proliferation [16, 17]. [score:4]
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[+] score: 3
For instance, miR-10 is required for hypermethylation in gastric cancer, and the mechanism was predicted by targeting the HOXA1 gene [6]. [score:3]
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[+] score: 3
Among these 21 differentially expressed miRNAs, 17 (miR-10b-5p, miR-223-3p, miR-208a-5p, miR-434-3p, miR-190a-5p, miR-30d-5p, miR-347, miR-493-5p, miR-29a-5p, miR-451-5p, miR-190b-5p, miR-466c-5p, miR-883-5p, miR-466b-1-3p, miR-21-3p, miR-3596c, miR3584-3p) were proven significant (P < 0.05) by qRT-PCR, one (miR-487b-3p) had a tendency to be significant (P = 0.06), and three (miR-138-2-3p, miR-1188-3p, miR-665) were not confirmed to be significant (Table  2). [score:3]
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[+] score: 2
Other miRNAs from this paper: rno-mir-10a, rno-mir-26a, rno-mir-26b, rno-mir-146a, rno-mir-146b
Moreover, the endocannabinoid system has come under scrutiny given that several microRNAs such as miR26, miR146, and miR10 are responsible for its gene regulation [28, 29]. [score:2]
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[+] score: 2
Other miRNAs from this paper: mmu-mir-10b
MicroRNA-10b Induces Vascular Muscle Cell Proliferation through Akt Pathway by Targeting TIP30. [score:2]
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[+] score: 2
Other miRNAs from this paper: rno-mir-191a, rno-mir-1, rno-mir-191b, rno-mir-155
miR-1, miR-10b, miR-155, and miR-191 are novel regulators of BDNF. [score:2]
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[+] score: 2
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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[+] score: 2
Indeed, when the data of the Yamaura’s study were compared with findings of the present study several miRNAs were regulated in common and included for blunt steatosis miR-10b and miR-183; similarly with NASH the miRNAs miR-17, miR148b-5p and miR-197 were commonly regulated thus providing independent evidence for their diagnostic utility in animal studies. [score:2]
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[+] score: 1
Circulating exosomal miR-21 has been reported as a biomarker in each tumor stage of colorectal cancer [15] and plasma exosomal miR-23b-3p, miR-10b-5p and miR-21-5p have been reported as prognostic biomarkers for non-small-cell lung cancer [16]. [score:1]
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Wu et al. [11] reported that the expression of certain miRNAs either increases (e. g., miR-182) or decreases (e. g., miR-10b) in parallel with DR progression in the retinas of rats with STZ -induced DM; however, no study has been conducted thus far to investigate miRNA variations in human retinal cells under prolonged HG exposure. [score:1]
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