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31 publications mentioning rno-mir-10a

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

1
[+] score: 165
Other miRNAs from this paper: mmu-mir-10b, hsa-mir-10a, hsa-mir-10b, mmu-mir-10a, rno-mir-10b
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 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]
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]
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]
By combining the RNA-seq and miRNA target prediction software results, BDNF was predicted to be a potential direct target of miR-10a/b in GCs (Fig. 5A). [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]
These results indicated that BDNF was a direct target of miR-10a and miR-10b in GCs. [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]
BDNF is a direct target of miR-10a/b in GCs. [score:4]
miR-10a and miR-10b expression in granulosa cells is regulated by extrinsic/intrinsic signals. [score:4]
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]
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]
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]
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]
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]
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]
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]
As shown in Fig. 5E, miR-10a/b overexpression led to a significant decrease in BDNF protein levels compared with the negative control. [score:2]
Taken together, these results suggest that miR-10a and miR-10b might play a negative role in follicle development. [score:2]
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]
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]
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]
The miR-10 family has two members, miR-10a and miR-10b. [score:1]
miR-10 family members repressed proliferation and induced apoptosis in granulosa cells. [score:1]
Additionally, the TGFβ pathway and miR-10a/b form a negative feedback loop in GCs. [score:1]
Both miR-10a and miR-10b were induced by TGF-β1 in GC. [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]
Taken together, the results showed that BDNF could at least partially mediate the function of the miR-10 family in GCs. [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]
Effects of exposure to hormone and growth factors on miR-10a and miR-10b in granulosa cells. [score:1]
BDNF rescues miR-10 family-caused effects in GCs. [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]
It was also reported that miR-10 could repress proliferation in porcine granulosa cells 19. [score:1]
miR-10a and miR-10b repress proliferation and induce apoptosis in human, mouse and rat granulosa cells. [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]
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]
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]
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]
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]
As expected, the mediator of FSH in GCs, cAMP, also greatly repressed miR-10a and miR-10b in GCs (Fig. 3A). [score:1]
The seed region (UCAAGUA) of miR-10 is conserved among vertebrate species. [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]
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 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]
In contrast, apoptosis was induced by miR-10a and miR-10b in GCs of different species (Fig. 2C). [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]
SVOG cells were collected 48 h after transfection with miR-10a/b mimics and/or negative control. [score:1]
BDNF rescues miR-10a- and miR-10b -induced proliferation repression and apoptosis induction in GCs. [score:1]
The effect of the miR-10 family on GCs on a transcriptome-wide scale. [score:1]
The nucleotide sequence of the miR-10a and miR-10b precursors are highly conserved in mammals (Fig. 1A). [score:1]
As expected, BDNF could rescue GC apoptosis caused by miR-10a and miR-10b mimic transfection (Fig. 6D). [score:1]
Therefore, we tested the effect of recombinant TGF-β1 on miR-10a/b in GCs. [score:1]
miR-10 was identified as a specific marker for mouse granulosa cells from previous miRNA-sequencing results 17. [score:1]
We also identified that miR-10a/b and the TGF-β pathway form a negative feedback loop in granulosa cells. [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]
The results showed that FGF9 could also greatly repress the miR-10 family in GCs (Fig. 3A). [score:1]
miR-10a and miR-10b mimic treatment significantly reduced the viability of human, mouse and rat GCs (Fig. 2A). [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]
Identification of miR-10a and miR-10b in granulosa cells. [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]
Additionally, many hormones and growth factors in the ovary repressed the miR-10 family in GCs. [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]
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]
Based on small RNA-seq from a previous study, miR-10 is a specific marker for mouse granulosa cells 17. [score:1]
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2
[+] score: 81
Other miRNAs from this paper: rno-mir-26a, rno-mir-103-2, rno-mir-103-1, rno-mir-495
Therefore, the goals of this study were to provide a potential mechanistic explanation for EtOH -induced effects on gene expression by quantifying the expression of EtOH sensitive miRs (miR-10a-5p, miR-26a, miR-103 and miR-495) during normal pubertal development in the male rat hippocampus, and then elucidate how peri-pubertal binge EtOH exposure alters the expression of those miRs. [score:8]
Therefore, we identified putative target genes of miR-10a-5p, miR-26a, miR-103 and miR-495 that were relevant to known dorsal and ventral hippocampus functions using target prediction software programs, Targetscan and MirDB. [score:7]
Therefore, we quantified the expression of miR-10a-5p, miR-26a, miR-103, and miR-495 in the ventral hippocampus across pubertal development in untreated rats to determine if there were region specific miR expression patterns in the hippocampus. [score:6]
Therefore, we first quantified the normal developmental expression profile of miR-10a-5p, miR-26a, miR-103 and miR-495 in the rat hippocampus at three time points in pubertal development (early, mid/peri, and late). [score:5]
org) [40], [41], [42], we identified brain-derived neurotrophic factor (BDNF) as a target gene of miR-10a-5p, miR-26a, miR-103 and miR-495, and sirtuin 1 (SIRT1) as a target gene of miR-26a, miR-103 and miR-495. [score:5]
Taken together our data revealed that the expression of each miR tested (miR-10a-5p, miR-26a, miR-103 and miR-495) is dynamic across pubertal development and that the developmental profiles for each miR are distinct between the dorsal and ventral hippocampus. [score:5]
Overall, our data reveal novel findings about the age and brain-region specific expression of miR-10a-5p, miR-26a, miR-103, and miR-495 during pubertal development in male rats. [score:4]
Therefore, we first determined the normal developmental profile of mature miR-10a-5p, miR-26a, miR-103 and miR-495 expression in the dorsal hippocampus using untreated male Wistar rats. [score:4]
Moreover, mid/peri-pubertal binge EtOH exposure altered normal pubertal development expression patterns of miR-10a-5p, miR-26a, miR-103, miR-495, Dicer, Drosha, BDNF and SIRT1 in an age- and brain region -dependent manner. [score:4]
For instance, miR-10a-5p expression decreased significantly between early and mid/peri-puberty, and remained lower than early puberty levels until late puberty (Fig. 2A, solid line). [score:3]
Mature miR-10a-5p, miR-26a, and miR-495 expression levels in the dorsal hippocampus of untreated male rats are age dependent. [score:3]
Our analysis of potential targets for each EtOH-sensitive miR identified a single putative binding site in the 3′UTR of BDNF for each miR-10a-5p, miR-26a, and miR-103 (Fig. 5). [score:3]
0083166.g003 Figure 3 miR-10a-5p (A), miR-26a (B), miR-103 (C), and miR-495 (D) expression levels in untreated (solid line) and EtOH -treated (dashed line) pubertal male rats. [score:3]
For instance, BDNF was identified as a putative target gene for miR-10a-5p, miR-26a, miR-103 and miR-495. [score:3]
Mature miR-10a-5p, miR-26a, miR-103, and miR-495 expression levels in the ventral hippocampus of untreated male rats are age -dependent. [score:3]
Repeated adolescent binge EtOH exposure differentially alters expression of miR-10a-5p, miR-26a, miR-103 and miR-495 in the ventral hippocampus. [score:3]
0083166.g002 Figure 2 miR-10a-5p (A), miR-26a (B), miR-103 (C), and miR-495 (D) expression levels in untreated (solid line) and EtOH -treated (dashed line) pubertal male rats. [score:3]
The mature expression levels of miR-10a-5p were significantly increased by an average of 3–5 fold following mid/peri-pubertal binge EtOH exposure (Fig. 3A, dashed line). [score:3]
Rats were administered our repeated binge-pattern EtOH exposure paradigm (see methods) and dorsal hippocampal miR expression of miR-10a-5p, miR-26a, miR-103 and miR-495 was compared with untreated rats/water -treated rats immediately following binge EtOH exposure and one-month post-EtOH exposure. [score:2]
Specifically, miR10a-5p showed no change between early and mid/peri-puberty, but significantly increased by late puberty in the ventral hippocampus (Fig. 3A, solid line). [score:1]
One example of a large fold change was observed with miR-10a-5p. [score:1]
There were no potential binding sites in the 3′UTR of SIRT1 for miR-10a-5p, but there was a single potential binding site for each of the other miRs tested (miR-26a, miR-103 and miR-495; Fig. 5). [score:1]
Indeed, there was a significant main effect of treatment and a significant interaction between age/treatment for miR-10a-5p, miR-103, and miR-495 in the ventral hippocampus (Table 2). [score:1]
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[+] score: 31
Acarbose may upregulate miR-10a-5p to suppress the expression of IL6 in the gut, thereby moderating glucose homeostasis and inflammation in diabetic rats. [score:8]
Il6 and Tnf were identified as target genes of miR-10a-5p, and Mapk1 was one of the target genes of miR-664. [score:5]
Thus, acarbose may moderate glucose metabolism and proinflammation by up -regulating miR-10a-5p and decreasing the expression of TNF-α. [score:4]
In conclusion, acarbose can regulate glucose metabolism through the MAPK pathway and can suppress of proinflammatory cytokines by increasing miR-10a-5p and miR-664 in the ileum. [score:4]
However miR-151*, miR-10a-5p, miR-205, miR-17-5p, miR-145 and miR-664 were up-regulated in the AcarH group (fold change>2, P<0.05, Table 2, Figure 4). [score:4]
TNF-α is another target gene of miR-10a-5p. [score:3]
These findings suggest that acarbose can reduce the expression of inflammatory cytokines in the ileum through miR-10a-5p and miR-664. [score:3]
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4
[+] score: 21
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Of the three ZT06 groups that illustrated differential expression of miRNAs due to CD, emphasis was placed on the two-week chronic ZT06 group due to the differential expression of miRs 146a and 146b, and miR-127 (Figures 5A-5B and 6A). [score:11]
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Differentially expressed miRNAs based on Illumina sequencing in all the circadian-disrupted samples and their links to breast cancer development and circadian rhythms. [score:10]
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5
[+] score: 18
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]
It was demonstrated in Zebrafish embryo that miR-10a∖b had high expression in endothelial cells and regulated blood vessel outgrowth during development. [score:5]
miR-10a∖b target mib1 and Notch signaling. [score:3]
MicroRNA-10a/10b represses a novel target gene mib1 to regulate angiogenesis. [score:3]
Our results suggest that endothelial cells might be a powerful source of EVs delivering miR-10a/10b after exercise. [score:1]
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6
[+] score: 11
In the time course of downregulation, miR-10a, -98, -99, and -124a showed a long duration (~24 hr) of downregulation, while miR-134 nearly fully recovered by this time (P > 0.05 compared to the basal level). [score:6]
The extent of downregulation can be categorized into three groups: one retaining less than 5% of the basal miRNA level in naïve animal (miR-10a, -98); one maintaining 5~15% (miR-99, -124a, -183) and one showing more than 25% left (miR-29a, -134). [score:4]
We were able to detect miR-10a, -29a, -98, -99a, -124a, -134, and -183, but not miR-122, miR-143, and miR-153 even after 50 cycles of PCR, although they were previously reported from TG via Northern analysis [11]. [score:1]
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7
[+] score: 10
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]
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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8
[+] 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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9
[+] score: 8
Poh et al. [14] reported the miRNA expression profile in prefrontal cortex after facial carrageenan injection and Bai et al. [16] detected the expression of several neuron-specific mature miRNAs including miR-10a, -29a, -98a and -134a in TGs of rats with facial complete Freund's adjuvant (CFA) injection. [score:5]
Bai et al. [16] first described mature miR-10a, -29a, -98, -99a, -124a, -134 and -183 expressions in the TGs of rats with inflammatory muscle pain induced by facial CFA injection. [score:3]
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10
[+] score: 7
To verify the accuracy of microarray results we chose a selection of miRNAs from up-regulated (miR-10a-5p, miR-196b-5p, miR-352 and miR-324-3p) and down-regulated (miR-128a-3p) categories for confirmation using the method. [score:7]
[1 to 20 of 1 sentences]
11
[+] score: 6
org) revealed several target sites for BDNF: miR-206-3p, miR-10a-5p, miR-1b, miR-195-5p, and miR-497-5p that were conserved in humans. [score:3]
In contrast, miR-1b decreased and there was no change observed in miR-10a-5p (Fig.   5a). [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]
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]
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12
[+] score: 6
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]
Additionally, sequencing analysis identified 8 individual sequences within the miR-10a/b family (unique sequences; Table 3) as having >2 fold detected difference (epicardium>endocardium) within the samples tested. [score:1]
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13
[+] score: 6
Indeed, miRNAs that were differentially expressed in stress are recognized biomarkers of mental health, including miR-10a-5p in depression 65, miR-219a-5p in schizophrenia 66 and miR-182 in fear memory, depression and synaptic plasticity 67. [score:3]
After adjusting p-values using the Benjamini and Hochberg correction 27, three miRNAs were differently expressed which included miR-182, miR-10a-5p and miR-124-3p (FDR p < 0.05). [score:3]
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14
[+] score: 6
In addition, has-miR-181c and has-miR-10a showed a trend towards higher expression levels in DCM samples (P > 0.05). [score:3]
In addition, hsa-miR-181c (P > 0.05) and hsa-miR-10a (P > 0.05) exhibited a trend of higher expression levels in DCM samples, but these differences did not reach statistical significance when compared with control samples (Fig. 9). [score:2]
Selected miRNAs (hsa-miR-10a, miR-19b, miR-181c, miR-302d and miR-340) were further quantified with TaqMan qRT-PCR. [score:1]
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15
[+] score: 6
Kidney enriched miR-10a and miR-192 were previously identified as potential circulating biomarkers of renal injury in rats [48], however miR-192 had high expression in multiple dog tissues and was not identified as kidney enriched in the current study. [score:3]
High expression in dogs was observed for cfa-miR-10a, -10b, -22, -181a, -191, -192, and -378 (Additional file 4: Figure S3). [score:3]
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16
[+] score: 5
As depicted in Fig 6, among the miRNAs elevated in serum in our study, LPS has been shown to increase expression of miR-10a, miR-100, miR-508/511, miR-30c, and miR-125b in human fibroblast-like synoviocytes [41], increase expression of miR-146a in a human monocyte cell line [42], and increase miR-21 in cultured murine monocytes [43]. [score:5]
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17
[+] score: 5
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]
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18
[+] score: 5
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-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-362, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, 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-26b, 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-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, hsa-mir-301b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-182, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-466d, rno-mir-344a-2, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-15a, rno-mir-762, mmu-mir-466c-3, rno-mir-29c-2, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Our study showed that no miRNA was different between males and females in adenoma-free mice, while 3 miRNAs (miR-10a, miR-125, and miR-130a) were differentially expressed in adenoma-bearing male and female mice. [score:3]
According to volcano-plot analyses, no miRNA was different in males and females from adenoma-free mice, whereas 3 miRNAs (miR-10a, miR-125, and miR- 130a) from adenoma-bearing mice showed intergender differences. [score:1]
In particular, miR-10a is related to estrogen dependent cancer promotion [112, 113], miR-130a both to the estrogen and HER2 pathways [114, 115], and miR-125 to HER2/erbb2 estrogen sensitive oncogene activation [116, 117]. [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: 5
For example, miR-17 [12] and miR-100 [13] were up regulated while miR-10a [14] and miR-205 [15] were downregulated during the osteogenic differentiation in bone mesenchymal stem cells of rats (rBMSCs). [score:5]
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[+] score: 4
Other miRNAs from this paper: rno-mir-30d, rno-mir-30a, rno-mir-96, rno-mir-183
For example, the miRNA designated as miR-10a by ABI is called miR-10a-5p by TargetScan. [score:3]
By this method, only one miRNA (miR-10A) could be linked to pain, reflecting the lack of miRNA literature in the pain field [23]. [score:1]
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[+] score: 4
The relative expression was normalized to that of miR-10a-3p and miR-124-3p, the two miRNAs showing the least variability across the samples according to Normfinder. [score:3]
For miRNA data normalization, miR-10a-3p and miR-124-3p were both used as endogenous controls because they present the least variability across the samples according to Normfinder [15]. [score:1]
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23
[+] score: 3
Among the 12 selected miRNAs, two were lung-specific (miR-195 and miR-200c), one was kidney-specific (miR-10a), and three were co-expressed in the lung and heart (miR-126, miR-143 and miR-145) as determined by HSD, OSI and two-fold criteria. [score:3]
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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
Other miRNAs from this paper: hsa-mir-10a
A novel NF-κB/YY1/microRNA-10a regulatory circuit in fibroblast-like synoviocytes regulates inflammation in rheumatoid arthritis. [score:3]
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26
[+] score: 3
For instance, lower expression levels of miR-200b, miR-152 and miR-10a were associated with increased DNA methylation in bladder cancer [16], and miR-10a was silenced by aberrant DNA methylation in gastric cancer [17]. [score:3]
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[+] score: 2
Longevinex exceeded the effect of resveratrol in 15 of the 25 miRNAs including miR-10a, miR-20b, miR-21. [score:1]
1 up 3.7 down 12 down 1.1 miR-10a up 6.4 up 5.2 up 3.5 down 116 down 1.6 snoRNA202 up 3.8 up 4.7 up 3.2 down 6 down 3 miR-27b down 1.4 up 1.9 up 3.2 up 1 up 1 miR-29c up 5.4 up 4.5 up 3.1 up 1.5 down 1.5 miR-345-5p up 14.3 up 31.7 up 2.4 down 4.7 up 1.1 rno-miR-24-1 down 25.3 up 1.2 up 2.1 down 1.2 down 1.9 miR-687 up 3.8 up 1.8 up 2 down 1.7 down 11.5 miR-27a up 34 up 12. [score:1]
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[+] score: 2
MicroRNA-10a binds the 5′UTR of ribosomal protein mRNAs and enhances their translation. [score:2]
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[+] score: 2
Other miRNAs from this paper: rno-mir-10b, 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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30
[+] score: 2
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-10b, 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
Cortex let-7c-1, miR-10a, miR-21, miR-124a-1, miR-128a, miR-135b, miR-150, miR-199a, miR-217, miR-329, miR-451. [score:1]
Olfactory bulb let-7b, let-7c-1, let-7c-2, miR-10a, miR-16, miR-17, miR-21, miR-22, miR-28, miR-29c, miR-124a-1, miR-124a-3, miR-128a, miR-135b, miR-143, miR-148b, miR-150, miR-199a, miR-206, miR-217, miR-223, miR-29b-1, miR-329, miR-331, miR-429, miR-451. [score:1]
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[+] score: 1
For example, rno_circRNA_003295 is potentially able to interact with rno-miR-206-3p, rno_circRNA_002441 with miR-144-3p, and rno_circRNA_012846 with rno-miR-10a-5p. [score:1]
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