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32 publications mentioning rno-mir-103-1

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-103-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 89
Other miRNAs from this paper: rno-mir-10a, rno-mir-26a, rno-mir-103-2, 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]
The most striking effects of mid/peri-pubertal binge EtOH exposure in the ventral hippocampus were observed in miR-103 and miR-495 expression, as their normal developmental expression levels at both mid/peri-puberty and late-puberty were opposite following mid/peri-pubertal binge EtOH exposure. [score:6]
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]
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]
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]
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]
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]
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]
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]
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]
In the dorsal hippocampus, a two-way ANOVA revealed a main effect of age on the expression levels of all miRs tested, except miR-103 (Table 1). [score:3]
The histone deacetylase sirtuin 1 (SIRT1) was also predicted by computer algorithms to be a putative gene target of miR-26a, mir-103 and miR-495. [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]
Genome-wide miR expression profiles revealed that the miRs investigated in this study, miR-103 and miR-26a, are among the top 15 most abundantly expressed miRs in the rodent hippocampus [59]. [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]
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]
In the ventral hippocampus, there was a significant main effect of age in the untreated animals on all four miRs tested, including miR-103, which previously did not show a significant change across pubertal development in the dorsal hippocampus (Table 2). [score:2]
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]
The ventral hippocampus levels of miR-103 and miR-495 had a similar profile. [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]
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]
miR-103 was not significantly altered by mid/peri-pubertal EtOH treatment in the dorsal hippocampus, similar to the results observed with age alone (Fig. 2C). [score:1]
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2
[+] score: 73
Other miRNAs from this paper: rno-mir-103-2, rno-mir-107, rno-mir-122, rno-mir-370, rno-mir-539
In cultured hepatocytes, we observed that only those over -expressing miRNA-107-3p showed the down-regulation of CPT1a protein expression, suggesting that in fact cpt1a is a real target gene for miRNA-107-3p, but not for miRNA-103-3p. [score:10]
In the in vivo study, resveratrol induced the down-regulation of miRNA-103-3p and miRNA-107-3p in the liver, which was accompanied by a reduced expression of SREBP1. [score:6]
Joven J. Espinel E. Rull A. Aragonès G. Rodríguez-Gallego E. Camps J. Micol V. Herranz-López M. Menéndez J. A. Borrás I. Plant-derived polyphenols regulate expression of mirna paralogs miR-103/107 and miR-122 and prevent diet -induced fatty liver disease in hyperlipidemic miceBiochim. [score:6]
In our in vitro study, the over -expression of miRNA-103-3p and miRNA-107-3p in hepatocytes led to an increased expression of SREBP1, suggesting that in fact they were positive regulators. [score:6]
In rats treated with resveratrol, we found a significantly decreased expression of miRNA-103-3p, miRNA-107-3p and miRNA-122-5p, which was paralleled by a significant decrease in SREBP1 protein expression. [score:5]
The present study provides new evidence showing that srebf1 is a target gene for miRNA-103-3p and miRNA-107-3p and cpt1a a target gene for miRNA-107-3p. [score:5]
In this context, the aim of the present study was to determine whether, as in the case of other polyphenols, this reduction in liver fat was mediated by changes in the expression of miRNA-122-5p, miRNA-103-3p and miRNA-107-3p, which represent more than 75% of total miRNAs in the liver [19, 21, 22, 23, 24, 25], as well as in their target genes. [score:5]
With regard to miRNA-103-3p and miRNA-107-3p, as indicated before in the Discussion section, computational analysis (miRecords) revealed complementarity between these miRNAs and the 3′UTR region of srebf1, suggesting that it can be a direct target gene. [score:4]
Taking all that into account, it may be said that miRNA-103-3p and miRNA-107-3p are involved as positive regulators in the effects of this polyphenol on SREBP protein expression [35]. [score:4]
MiRNA-103-3p, miRNA-107-3p and miRNA-122-5p were individually over-expressed in AML12 hepatocytes. [score:3]
It has been reported in the literature that different types of polyphenols, such as proanthocyanidins or a mixture extracted from Hibiscus sabdariffa, are able to modify the expression of miRNA-122-5p (a liver specific miRNA and the most abundant one) and the paralogs miRNA-103-3p and miRNA-107-3p in liver [16, 17, 18, 19]. [score:3]
According to the miRecords data base, cpt1a is a predicted target gene for miRNA-103-3p and miRNA-107-3p. [score:3]
In the present study, we observed that the expression of the three miRNA analysed (miRNA-103-3p, miRNA-107-3p and miRNA-122-5p) was significantly reduced in the liver of rats treated with resveratrol (Table 2). [score:3]
As far as the lipogenic pathway is concerned, miRecords data base showed that srebf1 was a predicted target gene for miRNA-103-3p and miRNA-107-3p and fasn for miRNA-122-5p. [score:3]
The targeted miRNA assay sequences were as follows (source miRBase): rno-miRNA-103-3p: 5′-AGCAGCAUUGUACAGGGCUAUGA-3′ rno-miRNA-107-3p: 5′-AGCAGCAUUGUACAGGGCUAUCA-3′ rno-miRNA-122-5p: 5′-UGGAGUGUGACAAUGGUGUUUG-3′PCR was performed in an iCycler™–MyiQ™ Real-time PCR Detection System (Applied Biosystems, Foster City, CA, USA). [score:2]
The targeted miRNA assay sequences were as follows (source miRBase): rno-miRNA-103-3p: 5′-AGCAGCAUUGUACAGGGCUAUGA-3′ rno-miRNA-107-3p: 5′-AGCAGCAUUGUACAGGGCUAUCA-3′ rno-miRNA-122-5p: 5′-UGGAGUGUGACAAUGGUGUUUG-3′ PCR was performed in an iCycler™–MyiQ™ Real-time PCR Detection System (Applied Biosystems, Foster City, CA, USA). [score:2]
Wilfred B. R. Wang W. X. Nelson P. T. Energizing mirna research: A review of the role of mirnas in lipid metabolism, with a prediction that miR-103/107 regulates human metabolic pathwaysMol. [score:2]
Hepatocytes in a confluence status of approximately 90%, were transfected with Lipofectamine RNAiMAX (Applied Biosystems, Foster City, CA, USA) prepared following the manufacturer’s protocol, with mirVana miRNA mimics of mmu-miRNA-103-3p, mmu-miRNA-107-3p and mmu-miRNA-122-5p (homologous to rno-miRNA-103-3p, rno-miRNA-107-3p and rno-miRNA-122-5p respectively) (Applied Biosystems, Foster City, CA, USA). [score:1]
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3
[+] score: 61
One particularly interesting finding is the upregulation of miR-103 and downregulation of its putative gene target Ptplb in brains. [score:9]
In the mature brain, however, upregulation of miR-103 may suppress BDNF synthesis in humans [65] and promote neuropathological processes in a mouse mo del of Alzheimer’s disease [66]. [score:8]
C, Prenatal stress elevated expression of miR-103, which coincides downregulation of its potential target Ptplb (mean ± SEM). [score:8]
Ptplb is a putative target for miR-103, which was upregulated by prenatal stress (Figure 4C). [score:6]
miR-103 is enriched in the cortex [61] and its expression increases during neurodevelopment, particularly cell differentiation [62], [63] and translation [64]. [score:6]
miR-103 -mediated inhibition of Ptplb translation may contribute to alterations in behavioural and neuronal plasticity in prenatally stressed offspring. [score:5]
The putative gene target of miR-103, Ptplb, is essential for biosynthesis of tyrosine phosphatase-like member b, which is involved in a wide range of neuronal functions, including synapse formation [70], disorders involving the frontal cortex such as Alzheimer’s disease [71], [72] and schizophrenia [73]. [score:5]
Altered miR-103 expression in the developing brain may therefore contribute to cognitive changes in adulthood. [score:3]
B, Table of putative target genes for modulated miRNAs (miR-103, miR-151, and miR-219-2-3p; p≤0.05) and their physiological functions. [score:3]
Moreover, significant changes in expression due to prenatal stress were found in miR-103 (down), miR-151 (down), and miR-219-2-3p (up). [score:3]
Ptplb and Dazap1 are targets for miR-103 and miR-219, respectively. [score:3]
The following miRNAs were analyzed (5′ to 3′): mirR-181 and miR-186 (dams); miR-103, miR-151, miR-323, miR-145, miR-425, miR-98 (newborns). [score:1]
Non-stress groups), as observed by microarray analyses, the following candidates were selected for verification by qRT-PCR analysis: miR-151, miR-145, miR-425 (all down) and miR-103, miR-323, miR-98 (up) (Figure 3C). [score:1]
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4
[+] score: 42
Balderman et al. showed that BMP2 increased Runx2 expression in vascular smooth muscle cells and promoted calcification through down -regulating miR-30b-5p 31. miR-103-3p, identified as a mechanosensitive and bone abundant miRNA, inhibited the differentiation of osteoblasts by directly targeting Runx2 32 and the proliferation of osteoblasts by targeting Cav1.2 33. [score:11]
The results showed that 14 miRNAs (miR-30a-5p, miR-30e-5p, miR-425-5p, miR-142-3p, miR-191a-3p, miR-215, miR-29b-3p, miR-30b-5p, miR-26a-5p, miR-345-5p, miR-361-5p, miR-185-5p, miR-103-3p) were down-regulated but no miRNA was up-regulated among above three altered miRNAs from microarray in OVX serum by normalizing to miR-25-3p (Fig. 3b). [score:7]
The clinical characteristics of the subjects were shown in Table 1. Among the detected miRNAs, miR-30b-5p showed significant down-regulation in both osteopenic and osteoporotic patients, while miR-103-3p and miR-142-3p were markedly down-regulated only in osteoporotic patients (Fig. 4a). [score:5]
And 3 of them (miR-30b-5p, miR-103-3p and 142-3p) were finally confirmed down-regulation in the serum of both OVX rats, postmenopausal osteoporotic patients and bedrest monkeys. [score:4]
As shown in Fig. 4c, miR-30b-5p, miR-103-3p and miR-142-3p were significantly down-regulated after bedrest, while miR-328-3p had no significant change. [score:4]
Three serum miRNA (miR-103-3p, miR-142-3p and miR-328-3p) were markedly down-regulated only in osteoporotic patients and miR-30b-5p decreased in both osteopenic and osteoporotic patients. [score:4]
We presumed the possible reasons as following: Firstly, miR-30b-5p and miR-103-3p were identified as ostemiRs in osteoblasts and osteocytes 30, while postmenopausal osteoporosis was mainly due to the over-activity of osteoclasts 34. [score:1]
miR-30b-5p and miR-103-3p were two osteogenesis-related miRNAs. [score:1]
Secondly, it had been shown that bone loss was partly compensated by increased osteobalstogenesis during estrogen deficiency 35. miR-30b-5p and miR-103-3p may involve in these processes. [score:1]
And the ROC analysis (Fig. 4d) showed considerable diagnostic value: 0.926 for miR-30b-5p (95% CI = 0.67–1.00, p < 0.0001), 0.796 for miR-103-3p (95% CI = 0.52–0.96, p = 0.0133), 0.950 for miR-142-3p (95% CI = 0.68–1.00, p < 0.0001). [score:1]
As shown in Fig. 4b, the AUC of miR-30b-5p was 0.793 (95% CI = 0.625–0.909, p = 0.0001), and 0.800 for miR-103-3p (95% CI = 0.607–0.926, p = 0.0004), 0.789 for miR-142-3p (95% CI = 0.599–0.918, p = 0.0023), and 0.874 for miR-328-3p (95% CI = 0.698–0.967, p < 0.0001). [score:1]
To access the potential diagnostic value of miR-30b-5p for bone loss (osteopenia and osteoporosis), and the value of miR-103-3p, miR-142-3p, miR-328-3p for osteoporosis, ROC analysis was conducted and the associated area under the curve (AUC) was used to confirm the diagnostic value of each miRNA. [score:1]
After adjusting for age, weight and height, miR-30b-5p, miR-103-3p, miR-142-3p and miR-328-3p were significantly positively correlated with H-BMD (total hip BMD) (r = 0.541, p = 0.001; r = 0.355, p = 0.039; r = 0.650, p < 0.001; r = 0.355, p = 0.039 respectively). [score:1]
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5
[+] score: 36
miR-103 is also upregulated during porcine adipogenesis, and its inhibition suppresses adipogenesis [26]. [score:8]
Notably, 23 circulating miRNAs (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were significantly downregulated in DIO mice but upregulated in DIO + LFD mice. [score:7]
In vivo, miR-103 is downregulated in the mature adipocytes of obese mice [26] and upregulated during the differentiation of human and murine pre-adipocytes [27, 28]. [score:7]
As shown in the Venn diagram in Fig.   7, notably, 23 of the 28 upregulated miRNAs in DIO + LFD mice (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were downregulated in the DIO mice. [score:7]
A 9-fold upregulation of miR-103 was noted during early adipogenesis in 3T3-L1 pre-adipocyte cells, and lipid droplet formation was accelerated when it was ectopically expressed [26]. [score:6]
Some of the circulating miRNAs identified in this study have also been reported in the adipose tissue of DIO mice or implicated in adipogenic processes [11– 13], including Let-7, miR-103, miR-15, the miR-17-92 cluster (miR-17, miR-20a, and miR-92a), miR-21, miR-221, and miR-30b. [score:1]
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6
[+] score: 22
0172429.g005 Fig 5 The expression levels of miRNAs miR-107, miR-181c, miR-103, miR-101, miR-29a, miR-21 and miR-9 expression levels were down-regulated in the serum of diabetic rats and IOMe -injected rats (A). [score:8]
The expression levels of miRNAs miR-107, miR-181c, miR-103, miR-101, miR-29a, miR-21 and miR-9 expression levels were down-regulated in the serum of diabetic rats and IOMe -injected rats (A). [score:8]
The expression levels of miR-107, miR-181c, miR-103, miR-101, miR-29a, miR-21 and miR-9 were significantly down regulated in the blood serum of diabetic and IOMe -injected rats (Fig 5A) whereas, the expression levels of these miRNAs are normally high. [score:6]
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7
[+] score: 21
Recent evidence has shown that cancer cells [53] downregulate their microRNA network by targeting DICER through the overexpression of the microRNAs miR-103 and miR-107. [score:8]
Moreover, the microRNAs miR-103, miR-107, miR-133a, miR-145, mir146a and miR-98, which presented altered expression at 7 days after SCI in both Liu's study [6] and ours, demonstrated significant alterations in the expression of their targets, according to De Biase et al. [7]. [score:7]
However, this mechanism likely does not apply to the present case because miR-103 and miR-107 appear to be downregulated following injury, and previous studies have not found significant changes in DICER or DROSHA expression [7]. [score:6]
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8
[+] score: 19
Other miRNAs from this paper: rno-mir-103-2
Stress Modulates the Expression of Ube2s/LOC365566Our previous work showed that prenatal stress exposure increased the expression of miR-103 that potentially targets Ube2s/LOC365566 [6]. [score:7]
stress was shown to increase miR-103 expression [6], which supports the present finding of Ube2s/LOC365566 down-regulation. [score:6]
Our previous work showed that prenatal stress exposure increased the expression of miR-103 that potentially targets Ube2s/LOC365566 [6]. [score:5]
A second pathway investigated here involved Ube2s/LOC365566, a gene targeted by miR-103. [score:1]
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9
[+] score: 11
miRNA expression profiling of lung tissues demonstrated differential expression of seven miRNAs, with downregulation of miR-344a-3p (−2.36-fold change) and upregulation of miR-103 (4.04-fold change), miR-22 (2.72-fold change), miR-30b-5p (1.51-fold change), miR-347 (1.95-fold change), miR-382 (2.82-fold change), and miR-3573-3p (3.32-fold change) (Figures 3A,B). [score:11]
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10
[+] score: 11
In this sense, by virtue of miRNAs known mechanism of action, reducing gene expression by binding to the 3'UTR of their targeted genes, a number of evidenced miRNA species (Mir-27a, Mir-103, Mir-17-5p and Mir-130a) might be involved in turning off the 'neuron projection morphogenesis' process in the SHVT group. [score:5]
Other deregulated biological processes included ‘blood vessel development’ (Mir-155, Mir-17-5p and Mir-130a) (FDR = 6x10 [-4]), 'lung development' (Mir-17-5p and Mir-27a) (FDR = 4x10 [-4]), and ‘cell motion’ (Mir-103) (FDR = 8x10 [-4]) (S3 Table). [score:3]
A heatmap built from nominally significant miRNAs between SHVT and NA detected by sRNA-seq are shown in S3 Fig. When comparing the direct sequencing of the samples with the bioinformatic prediction, 28 miRNA species overlapped, from which Mir-27a, Mir-103, Mir-17-5p, Mir-130a, and Mir-155 were nominally significant although the abundance of the latter was observed to be opposite to the one deduced by GSEA (Table 2). [score:2]
Interestingly, this process was the only one involving all four miRNA species with a consistent abundance among microarray -based predictions and sRNA-seq experiments (Mir-27a, Mir-103, Mir-17-5p and Mir-130a) (FDR<1x10 [-4]) (S3 Table). [score:1]
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11
[+] score: 9
In response to 4 hours of mechanical stretch, rno-miR-322, let-7f, miR-103, miR-126, miR-494, miR-126*, miR-130b and miR-195 were significantly dysregulated (Fig.   7A and Supplementary Dataset  5), so we sought potential mRNA targets for these dysregulated miRNAs among the stretch-regulated genes in 4 and 12 hours timepoints. [score:6]
In response to 1 hour of mechanical stretching, only one miRNA, rno-miR-130b showed differential expression compared to controls (P < 0.05), whereas 8 miRNAs (rno-miR-322, rno-let-7f, rno-miR-103, rno-miR-126, rno-miR-494, rno-miR-126*, rno-miR-130b, rno-miR-195; P < 0.05) were dysregulated in response to 4 hours of stretch (Supplemental Dataset  5). [score:3]
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12
[+] score: 9
The expression of miR-122, miR-93, miR-103, miR-107, miR-206, miR-143, miR-24, and miR-106b were reduced upon treatment with Tg and Tm in H9c2 cells. [score:3]
We observed that changes in the expression of nine miRNAs (miR-24, miR-25, miR-7a, miR-103, miR-17-5p, miR-106b, miR-93, miR-206 and miR-133b) analyzed by qRT-PCR were consistent with those by miRNA microarray at p < 0.05 (Figure 3). [score:3]
We found that expression of many miRNAs (miR-24, miR-25, miR-7a, miR-103, miR-17-5p, miR-106b, miR-93, miR-206 and miR-133b) changed significantly during conditions of UPR in cardiomyoblasts. [score:3]
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13
[+] score: 8
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-18a, hsa-mir-21, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-30a, mmu-mir-99a, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-138-2, hsa-mir-192, mmu-mir-204, mmu-mir-122, hsa-mir-204, hsa-mir-1-2, hsa-mir-23b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-138-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-103-1, mmu-mir-103-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-26a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-26a-2, hsa-mir-376c, hsa-mir-381, mmu-mir-381, mmu-mir-133a-2, rno-let-7a-1, rno-let-7a-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-18a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-26a, rno-mir-30a, rno-mir-99a, rno-mir-103-2, rno-mir-122, rno-mir-126a, rno-mir-133a, rno-mir-138-2, rno-mir-138-1, rno-mir-192, rno-mir-204, mmu-mir-411, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-193b, rno-mir-1, mmu-mir-376c, rno-mir-376c, rno-mir-381, hsa-mir-574, hsa-mir-652, hsa-mir-411, bta-mir-26a-2, bta-mir-103-1, bta-mir-16b, bta-mir-18a, bta-mir-21, bta-mir-99a, bta-mir-126, mmu-mir-652, bta-mir-138-2, bta-mir-192, bta-mir-23a, bta-mir-30a, bta-let-7a-1, bta-mir-122, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-204, mmu-mir-193b, mmu-mir-574, rno-mir-411, rno-mir-652, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-1-2, bta-mir-1-1, bta-mir-133a-2, bta-mir-133a-1, bta-mir-138-1, bta-mir-193b, bta-mir-26a-1, bta-mir-381, bta-mir-411a, bta-mir-451, bta-mir-9-1, bta-mir-9-2, bta-mir-376c, bta-mir-1388, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-451b, bta-mir-574, bta-mir-652, mmu-mir-21b, mmu-mir-21c, mmu-mir-451b, bta-mir-411b, bta-mir-411c, mmu-mir-126b, rno-mir-193b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The qRT-PCR data showed similar expression trend of detected expression of these miRNAs from the library except miR-103. [score:5]
To validate above miRNA expression patterns, quantitative RT-PCR was performed on tissue-specific miRNAs (miR-122, -133a), high cloning frequency miRNAs (miR-26a, -99a and -150) and low cloning frequency miRNAs (miR-103, -107, -411, -423-5p, -574-3p and -652). [score:3]
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14
[+] score: 8
It was shown that human miR-103-3p was suppressed in EAT of coronary artery disease patients is one of the possible mechanisms targeting a chemokine CCL3 in EAT (Pisitkun et al., 2004). [score:7]
miR-103-3p was studied in epicardial adipose tissue (EAT), which is important for obesity, intra-abdominal visceral fat, and insulin resistance. [score:1]
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15
[+] score: 7
Expression was normalized to miR-103 as suggested by the “Norm-finder” algorithm, a mo del -based variance estimation predicting the stability of a given miRNA across samples [42]. [score:3]
The qPCR data for the technical confirmation were analyzed using the 2 [–ΔΔCt] quantitative method [40] where ΔΔCt = (Ct [target] - Ct [miR-103]) [SAH] - (Ct [target] - Ct [miR-103]) [Sham] and statistically evaluated by one-way ANOVA followed by Student’s t-tests. [score:3]
The selection of miR-103 for normalization was made by subjecting the data from the technical confirmation to the “Norm-finder” algorithm. [score:1]
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[+] score: 7
Other miRNAs from this paper: rno-mir-103-2, rno-mir-132, rno-mir-139, rno-mir-214, rno-mir-487b
Our group also identified another miRNA, miR-103-3p, that inhibited osteoblast proliferation and L-type calcium channel function mainly through suppressing Cav1.2 expression under a simulated microgravity environment 31 44. [score:7]
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17
[+] score: 6
For example, in the spinal nerve ligation mo del, intrathetal injections of miR-21 (Sakai and Suzuki, 2013), miR-103 (Favereaux et al., 2011), miR-183 (Lin et al., 2014) or of miR-195 inhibitor (Shi et al., 2013), and injection of miR-7a into the L5-DRG (Sakai et al., 2013) attenuate pain. [score:3]
Bidirectional integrative regulation of Cav1.2 calcium channel by microRNA miR-103: role in pain. [score:3]
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[+] score: 6
Other miRNAs from this paper: rno-mir-103-2, rno-mir-122
Relative quantification of PCR products was based on differences between miR-103 and the target using the comparative C [t] method (TaqMan Gold RT-PCR manual; PE Biosystems, Foster City, CA, United States) (Livak and Schmittgen, 2001). [score:3]
Semi-quantitative Real-time RT PCR quantification was performed using miR-103 as an internal control, since C [t] values of miR-103 did not differ between intrauterine conditions or after administration of miR-122 inhibitor, mimic, or scrambled sequence. [score:3]
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[+] score: 6
MicroRNA-103-1 selectively downregulates brain NCX1 and its inhibition by Anti-miRNA ameliorates stroke damage and neurological deficits. [score:6]
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[+] score: 6
The endogenous reference (miR-103) was chosen from the microarray expression data set on the basis of the following criteria: uniform and relatively high expression levels in all brain regions and hemispheres. [score:5]
Normalization was done with miR-103 (part # 4373158) as an endogenous control and the abundance of each miRNA was determined using the relative standard curve method. [score:1]
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[+] score: 6
Other miRNAs from this paper: rno-mir-16, rno-mir-103-2, rno-mir-122, rno-mir-191a, rno-mir-191b
From a theoretical perspective, the group of genes, 5S, miR-16, miR-103, miR-191, miR-Let7a and RNU48, and the group of genes, 18S, B2M, HPRT1 and SDHA, can be used for microRNA and for mRNA expression data normalization in our mo dels of acute hepatotoxicity, respectively, because they showed no expression differences. [score:5]
Four microRNAs (miR-16, miR-103, miR-191 and miR-Let7a) and three small RNA genes (5S, U6 and RNU48) were selected as candidate RGs for the normalization of the microRNA RT-qPCR data. [score:1]
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[+] 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-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-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, rno-mir-708, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-486b, rno-mir-126b, hsa-mir-451b, hsa-mir-499b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-130c, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, hsa-mir-486-2, mmu-mir-129b, mmu-mir-126b, rno-let-7g, rno-mir-148a, rno-mir-196b-2, rno-mir-486
By 18 wks of E [2] treatment, the mammary glands were characterized by lobular involution and hyperplasia, and only 1 miRNA was down-regulated (miR-139) and 5 miRNAs were up-regulated (miR-20b, miR-21, miR-103, mir-107, miR-129-3p, and miR-148a). [score:5]
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[+] score: 4
The results showed that miR-208, miR-124, miR-146a-5p, miR-103, and miR-21 were all expressed abnormally in spinal tissue of ASCI rats (Figure 2). [score:3]
In the ASCI group, the levels of miR-208, miR-124, and miR-146a-5p were decreased, while the levels of miR-103 and miR-21 were increased. [score:1]
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[+] score: 3
GRN expression is also under the post-transcriptional control of miR-107 (a member of a miRNA group also including miR-15, miR-16, miR-103, miR-195, miR-424, miR-497, miR-503, and miR-646), with implications for brain disorders (Wang et al., 2010). [score:3]
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[+] score: 3
Chronic ethanol feeding was observed to alter the expression levels of several miRNAs during liver regeneration, including miR-34a, miR-103, miR-107, miR-122 (11) and miR-21 (12). [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-100, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-9-2, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-184, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-205, mmu-mir-206, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-214, hsa-mir-219a-1, hsa-mir-223, mmu-mir-302a, hsa-mir-1-2, hsa-mir-23b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-184, hsa-mir-206, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-103-1, mmu-mir-103-2, rno-mir-338, mmu-mir-338, rno-mir-20a, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-100, mmu-mir-181a-1, mmu-mir-214, mmu-mir-219a-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-372, hsa-mir-338, mmu-mir-181b-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-100, rno-mir-103-2, rno-mir-107, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-145, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-184, rno-mir-199a, rno-mir-205, rno-mir-206, rno-mir-181a-1, rno-mir-214, rno-mir-219a-1, rno-mir-219a-2, rno-mir-223, hsa-mir-512-1, hsa-mir-512-2, rno-mir-1, mmu-mir-367, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, rno-mir-17-2, hsa-mir-1183, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-103b-1, hsa-mir-103b-2, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-219b, hsa-mir-23c, hsa-mir-219b, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, mmu-mir-219b, mmu-mir-219c, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Similarly, miR-17, miR-20a, miR-21, miR-16, miR-103, and miR-107 identified in A2B5-GalC+ cells showed overlapping expression with our OPs. [score:3]
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[+] score: 3
As shown in Fig 2, the levels of miR-126, 145 and 150 were similar when normalized to either a C. elegans miR39 standard or an internal miR-103 control (Fig 2). [score:1]
We note that the aforementioned study normalized their qPCR results to a C. elegans control, whereas we normalized our qPCR to an internal miR-103 control. [score:1]
As internal controls, U6 small nuclear RNA for tissue RNAs, and miR-103 for plasma RNAs were used. [score:1]
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[+] score: 2
And Mir375 is one of a number of involved in insulin synthesis and secretion (for instance Mir9 and Mir29a/b/c), insulin sensitivity in target tissue (Mir143 and Mir29) or glucose and lipid metabolism (Mir103/107 and Mir122) and thus, having potential roles in diabetes [see for instance, [52], [53]. [score:2]
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[+] score: 1
Previous reports have indicated miR-103 and miR-1a-3p modulate neuropathic or cancer pain through Cav1.2 calcium channel and clcn3, respectively [11], [28]. [score:1]
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[+] score: 1
These include miR-103 [18], miR-124 [20], miR-23b [21] and miR-7a [22]. [score:1]
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[+] score: 1
In addition to let-7 and miR-23b, other miRNAs involved in morphine tolerance include miR-124, miR-190, miR-103 and miR-93-5p [14– 17]. [score:1]
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[+] score: 1
The eight circulating miRNAs, miR-29a, miR-34a, miR-375, miR-103, miR-107, miR-132, miR-142-3p and miR-144, and the two tissue-specific miRNAs, miR-199a-3p and miR-223, were identified to be significantly altered in T2D across a meta-analysis of controlled profiling studies [51]. [score:1]
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