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35 publications mentioning rno-mir-183

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-183. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 103
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, 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-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, 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-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
The expression levels of miR-183, miR-96, and miR-182 were most highly up-regulated, whereas miR-122, miR-503, and miR-139-3p exhibited the greatest down-regulation as a result of 17α-E2 treatment. [score:9]
ACTH up-regulated the expression of miRNA-212, miRNA-182, miRNA-183, miRNA-132, and miRNA-96 and down-regulated the levels of miRNA-466b, miRNA-214, miRNA-503, and miRNA-27a. [score:9]
The expression levels of miR-183 (4.61-fold), miR-96 (4.56-fold), and miR-182 (4.29-fold) were most highly up-regulated, whereas miR-122 (9.79-fold), miR-503 (5.88-fold), and miR-139-3p (1.94-fold) showed the greatest down-regulation as a result of 17α-E2 treatment. [score:9]
Real-time PCR (qRT-PCR) measurements demonstrated that ACTH treatment upregulated the expression of miRNA-212, miRNA-183, miRNA-182, miRNA-132 and miRNA-96, while down -regulating the expression of miRNA-466b, miRNA-214, miRNA-503 and miRNA-27a. [score:7]
qRT-PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats (Fig. 3 ). [score:7]
The levels of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377, and miRNA-96 were up-regulated, whereas miR-125b, miRNA-200b, miR-122, miRNA-466b, miR-138, miRNA-214, miRNA-503 and miRNA27a were down-regulated in response to 17α-E2 treatment. [score:7]
Real-time quantitative PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats. [score:7]
Treatment of MLTC-1 cells with Bt [2]cAMP for 6 h increased the expression of miRNA-212, miRNA-183, miRNA-132, miRNA-182 and miRNA-96, and inhibited the expression of miRNA-138 and miRNA-19a. [score:7]
Treatment of MLTC-1 cells with Bt [2]cAMP for 6 h increased the expression of miRNA-212, miRNA-183, miRNA-132, miRNA-182 and miRNA-96 and inhibited the expression of miRNA-138 and miRNA-19a (Fig. 4B ). [score:7]
Bt [2]cAMP stimulation of granulosa cells caused down-regulation of a majority of miRNAs, including miRNA-200b, miRNA-466b, miRNA-27a, miRNA-214, miRNA-138 and miRNA-19a, but expression levels of miRNA-212, miRNA-183, miRNA-182, and miRNA-132 were significantly increased. [score:6]
qRT-PCR measurements indicated that exposure of primary rat granulosa cells to Bt [2]cAMP for 24 h inhibited the expression of miRNA-200b, miRNA-466b, miRNA-27a, miRNA-214, and miRNA-138 and miRNA-19a while enhancing the expression of miRNA-212, miRNA-183, miRNA-182, and miRNA-132 (Fig. 4 ). [score:5]
Microarray data demonstrated that the levels of miR-183 and miR-182 were up-regulated with 17α-E2 treatment, but not with ACTH (p = 0.065) treatment; qRT-PCR measurements, however, showed significant increases in their expression in response to either ACTH or 17α-E2 treatment. [score:4]
Real-time PCR (qRT-PCR) confirmed ACTH -mediated up-regulation of miRNA-212, miRNA-183, miRNA-182, miRNA-132 and miRNA-96. [score:4]
We next evaluated the effects of Bt [2]cAMP stimulation of rat ovarian granulosa cells and of mouse MLTC-1 Leydig tumor cells on the expression of twelve miRNAs (miRNA-212, miRNA-122, miRNA-183, miRNA-200b, miRNA-466b, miRNA-182, miRNA-96, miRNA-27a, miRNA-132, miRNA-214, miRNA-138 and miRNA-19a) whose adrenal expression was differentially altered in response to treatment of rats with ACTH, 17α-E2 or DEX. [score:3]
MiR-183, miR-96 and miR-19a were predicted to target the ABCA1 gene. [score:3]
The levels of expression of miRNA-212, miRNA-122, miRNA-138, miRNA-214, miRNA-183, miRNA-182, miRNA-132, miRNA-96, miRNA-466b, miRNA-200b, and miRNA-19a are shown. [score:3]
More specifically, we assessed the impact of Bt [2]cAMP treatment on the expression of miRNA-212, miRNA-122, miRNA-27a, miRNA-466b, miRNA-200b, miRNA-138, miRNA-214, miRNA-183, miRNA-182, miRNA-132, miRNA-96 and miRNA-19a. [score:3]
0078040.g003 Figure 3Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
Dexamethasone treatment decreased miRNA-200b, miR-122, miR-19a, miRNA-466b and miRNA27a levels, but increased miRNA-183 levels. [score:1]
Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
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2
[+] score: 28
Notably, we found miR-222, miR-291-3p, miR-183, miR-363-3p, miR-92, miR-19a and miR-145 as down-regulated miRNAs between E11 and E13 and whose expression was negatively correlated with the expression of their predicted targets. [score:10]
Focusing on the down-regulated miRNAs that had a significant negative correlation in Figure 6, we performed network analysis and identified miR-92, miR-183, miR-222 and miR-291-3p as predicted to target multiple TFs that were up-regulated in E13 ENPs (Figure 8). [score:9]
Additional support for this hypothesis was provided by the miRNA-TF mRNA network analysis in Figure 8. We found four down-regulated miRNAs (miR-92, miR-183, miR-222 and miR-291-3p) that were predicted to target multiple TFs, which were up-regulated in E13 ENPs. [score:9]
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3
[+] score: 28
The final stable reporter cell line was designed to identify small compounds (e. g. HDAC inhibitor Panobinostat) that inhibit miR-182 (and/or miR-183) generation or function, thereby resulting in the activation of the luciferases (both firefly and Renilla). [score:5]
We used a miR-182 (or miR-183) inhibitor (miRIDIAN microRNA hairpin inhibitor, Thermo Fisher Scientific) as a positive control and non-specific miRNA (miRIDIAN microRNA Negative Control, Thermo Fisher Scientific) as a negative control. [score:5]
Starting from these two vectors, we built a dual reporter construct with the miR-182 (or miR-183) target sequence (Figure 1 and Supplementary Figure 1), so that the presence of mature miR-182 or miR-183 would lead to a decrease in luciferase (both firefly and Renilla) signal, enabling the detection of putative miR-182 (or miR-183) levels. [score:3]
In order to maintain minimal basal levels of luciferase activities, we transduced these stable cell lines with lentiviral particles containing miR-182 (or miR-183) shMIMIC microRNAs (Thermo Fisher Scientific), and in so doing established cell lines that constitutively expressed these miRNAs via the selective pressure of puromycin. [score:3]
We then examined whether these stable transfectants (miR-182 or miR-183 target sequence in pmirGLO/psiCHECK1 plus lentiviral particles containing miR-182 or miR-183 shMIMIC) were usable for high-throughput screens. [score:3]
The final stable reporter cell line was designed to identify small compounds that inhibit miR-182 (and/or miR-183) generation or function, thereby resulting in the activation of the luciferases (both firefly and Renilla). [score:3]
As shown in Supplementary Figure 2(c), the basal level of luciferase activities (both firefly and Renilla) are very low in comparison to negative controls in Supplementary Figure 2(a) and (b) and the activation by the miR-182 (or miR-183) inhibitors were substantial. [score:3]
The established stable transfectants responded well to both miR-182 or miR-183 mimics (i. e. the transfection of these mimics caused the depression of both firefly and Renilla luciferase acitivities in each cell line (Supplementary Figure 2b)). [score:1]
Of note, the endogenous levels of both miR-182 and miR-183 are quite low in SHSY5Y cells and thus the basal levels of luciferase activities are quite high (Supplementary Figure 2a and b). [score:1]
We confirmed that the presence of mature miR-182 or miR-183 would lead to a decrease in luciferase (both firefly and Renilla) signal, enabling the detection of putative miR-182 (or miR-183) levels (Supplementary Figure 2). [score:1]
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4
[+] score: 28
miR-146a-5p, miR-155-5p, miR-147b, and miR-223-3p were downregulated, while miR-182-5p, miR-183-5p, and miR-9-3p were upregulated. [score:7]
In murine EAU or human sympathetic ophthalmia eyes, miR-182 and miR-183 were downregulated following disease induction and were speculated to be associated with retinal tissue injury [27] and Forkhead box O1 or Fas/Fas ligand system activation [26, 53]. [score:6]
Among the miRNAs studied, miR-146a-5p, miR-155-5p, miR-182-5p, and miR-183-5p are four particularly crucial miRNAs for the following reasons: they all show significant differential profiles in the disease course; they all regulate NF- κB pathway, and miR-146a-5p and miR-155-5p are regarded as potent immunological drivers; they all have been reported in some uveitis mo dels. [score:4]
No significant difference was noted in terms of miR-182-5p and miR-183-5p in the popliteal lymph nodes over the course of the disease. [score:3]
The complete dynamic profiles of the levels of each miRNA are summarized in Table 1 and Figure 2. Generally, the expression of miR-9-3p, miR-182-5p, and miR-183-5p tended to increase from day 7 after immunization onwards and peaked at day 10 after immunization. [score:3]
The expression levels of miR-146a-5p, miR-155-5p, miR-182-5p, and miR-183-5p in iris/ciliary bodies and popliteal lymph nodes are shown in Figure 3. The levels of miR-146a-5p and miR-155-5p in the popliteal lymph nodes reached their lowest point earlier, on day 7, while those in the iris/ciliary body tissue kept decreasing until day 15 after immunization. [score:3]
The eight miRNAs studied were miR-155b-5p, miR-21-5p, miR-146a-5p, miR-9-3p, miR-147b, miRNA-183-5p, miRNA-182-5p, and mi -RNA-223-3p. [score:1]
MiR-182 and miR-183 belong to the same family, and unlike other miRNAs, miR-182 is one of the few dominant miRNAs that can increase more than 100-fold [48]. [score:1]
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5
[+] score: 26
rno-miR-675-5p 4.143757751 Premature senescence of cardiac progenitor cells, G1 arrest, reduced cell proliferation, colony formation, migration and invasion rno-miR-183-3p 3.74730108 Regulates claudin-1 expression rno-miR-299a-5p 3.626723224 Anti-apoptotic role rno-miR-200c-3p 3.593610443 Targets the VEGF-VEGFR2 pathway and angiogenesis rno-miR-665 3.511737089 Negatively targets anti-apoptotic BCL2L1 rno-miR-291a-5p 3.457928187 VSMC migration rno-miR-490-5p 2.373358 Tumour suppressor rno-miR-1 2.505729 Suppresses cell growth rno-miR-133b 2.192279 Inhibits cell proliferation and invasion rno-miR-30c-1-3p 2.70761 Suppresses PXR expression rno-miR-294 2.010496 Promotes proliferation and differentiation rno-miR-127-5p 2.780488 A regulator of MMP-13 and suppresses cell growth rno-miR-503 2.327383 Inhibits cell proliferation and invasion Table 2 Twenty down-regulated miRNAs. [score:26]
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6
[+] score: 26
In a recent study, miR-183 and miR-96 were observed a significant down-regulation with the increase of Nav1.3 expression in L5 DRG after SNL, which were abundant in DRG neurons (Aldrich et al., 2009; Lin et al., 2014), overexpression of miR-183 and miR-96 were capable to attenuate neuropathic pain by repressing Nav1.3. [score:8]
Using Target Scan software, miR-30b, miR-96, miR-183, and miR-132 were found to target SCN3A. [score:5]
MiR-132 was upregulated in SNI rats (Leinders et al., 2016), while miR-182, miR-183, miR-96 decreased in SNL rats (Aldrich et al., 2009). [score:4]
Using Target Scan software, miR-30b, miR-96, mir-183, and miR-132 were predicted to highly relate to SCN3A. [score:3]
Intrathecal miR-183 delivery suppresses mechanical allodynia in mononeuropathic rats. [score:3]
SCN3A was not only targeted by miR-30b, but also controlled by miR-183 and miR-96 in SNL rat DRGs (Aldrich et al., 2009). [score:3]
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7
[+] score: 23
The unique miRNA expression patterns distinguishing the ASH group from the control group were composed of six downregulated (miR-199a-3p, miR-214, miR-93, miR-146a, miR-191 and let-7b) and six upregulated (miR-129, miR-490, miR-21, miR-503, miR-183 and miR-185) miRNAs. [score:9]
Dolganiuc et al (13) demonstrated that the Lieber-deCarli alcohol diet upregulated 1% of known miRNAS, including miR-705 and miR-1224, and downregulated 1% of known miRNAs, including miR-182, miR-183 and miR-199a-3p in mice with alcoholic steatohepatitis compared with pair-fed controls. [score:6]
The expression levels of nuclear receptor subfamily 3, group C, member 1 (glucocorticoid receptor, nr3c1), which was also identified to be regulated by miR-183, may be associated with alcohol abuse (37). [score:4]
MiR-183 may inhibit tumor necrosis factor receptor superfamily, member 8 (TNFRSF8, also termed CD30) expression, a marker of cells producing Th2 (T-helper-2)-type cytokines, and the Th2-type cytokine profile has been documented in ALD (36). [score:4]
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8
[+] score: 21
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-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-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-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
Unlike other miRNAs in DHT -treated PCOS rats, miR-183 was found to be highly expressed in granulosa cells of control ovaries but was down-regulated by 10-fold in the PCOS counterpart. [score:6]
Thus, it is possible that the down-regulation of miRNAs (rno-miR-770, rno-miR-466c, rno-miR-31, rno-miR-183, rno-miR-96, rno-miR-132, rno-miR-182, rno-miR-384-3p and rno-miR-184) observed in this study could be associated with promoted thecal hyperandrogenesis [37, 38]. [score:4]
MiRNAs found to be primarily down-regulated in DHT -treated rats includes rno-miR-770, rno-miR-466c, rno-miR-21, rno-miR-31, rno-miR-182, rno-miR-183, rno-miR-96, rno-miR-132, rno-miR-182, rno-miR-384-3p and rno-miR-184. [score:4]
Among the fourteen miRNAs mapped to the ingenuity databases, twelve (rno-let-7d, rno-miR-132, rno-miR-182, rno-miR-183, rno-miR-184, rno-miR-21, rno-miR-221, rno-miR-24, rno-miR-25, rno-miR-26b, rno-miR-31 and rno-miR-96) had 171 experimentally validated targets. [score:3]
Whereas rno-miR-24 and rno-miR-183 were highly expressed in the theca and, to a lesser extent, in the granulosa cells of the cystic follicles (Figure  5), Rno-miR-31 and rno-miR-96 were present in the cumulus granulosa cells. [score:3]
These included rno-miR-24, rno-miR-31, rno-miR-96, rno-miR-183, rno-miR-222, rno-miR-489, U6 snRNA (positive control) and scrambled miRNA (negative control). [score:1]
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9
[+] score: 20
A single miRNA (miR-183) showed sex-biased expression at 104 weeks of age and was expressed at levels 17.2 times higher in males than females. [score:5]
The expression of miR-183 exhibited the largest identified sex difference with 17.2-fold higher expression in males compared to females at 104 weeks of age. [score:4]
miR-183 and miR-96 are co-transcribed from the miR-183-96-182 cluster found on chromosome 4 in rats and chromosome 7 in humans [64], suggesting that post-transcriptional processing may independently control the expression of these miRNAs. [score:3]
miRNAs showing the most male-biased expression included miR-125b-5p, miR-99a*, miR-99a, miR-96, miR-221, and miR-183 (Fig.   3). [score:3]
This was the second highest fold change difference among all sex-biased miRNAs, with only male biased miR-183 having a greater sex-biased expression (17-fold). [score:3]
MiR-183 has been shown to function in a pro-oncogenic manner by suppressing apoptosis and promoting proliferation in esophageal cancer cells [65]. [score:2]
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10
[+] score: 18
miRNAs that had approximately 2-fold upregulation included members of miR-29 family and miR-34 family and that were downregulated by about 2-fold were members of the miR-181 family and miR-183 family. [score:7]
In vertebrates, the expression domain of conserved miRNA-183 (miR-183) family members appears to be restricted to ciliated neurosensory epithelial cells and certain cranial and spinal ganglia [26, 27]. [score:3]
Additionally, expression of miR-183 family members in mouse eye and aural sensory hair cells of the ear has been previously demonstrated [29]. [score:3]
In zebrafish the miRNAs are detected in the eye, nasal epithelium, and sensory hair cells of the ear and neuromasts [26], and injection of miR-183 and miR-200 family members into zebrafish embryos have been demonstrated to impact development and affect neuromast migration [28]. [score:2]
The inconsistency between Zhang’s report and our study suggested that miRNA patterns in the organ of Corti change with aging and that miRNAs such as miR-183 and miR29 play different roles in the development of organ of Corti in newborn, younger and older animals. [score:2]
miRNAs that increased mostly in the adult basilar membrane includes miR-296, mi-130b and miR-183 and that those that decreased mostly include miR-29c and miR-29a. [score:1]
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11
[+] score: 14
According to our IPA networks, the downregulation of miR-183 could also promote BDNF expression (see Figure 7, network 4), whereas the downregulation of miR-329 and miR-331 may induce the overexpression of sema3. [score:11]
Specifically, miR-Let7a, miR-107, and miR-183 have been described as regulators of cell death, and miR-181b and miR199 are involved in the control of inflammation (see file S6). [score:2]
Specifically, BDNF is related to miR-183, semaphorin 3 to miR-329 and miR-331, Neuritin-1/ nrn1 to miR-331 and miR-342 and Ephrin-B2/ efnb2 to miR-340 and miR-294. [score:1]
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12
[+] score: 12
Stress also downregulated miRNAs that possess potential roles in the pathogenesis of psychiatric diseases, such as miR-96 [51], miR-182 and miR-183 [52]. [score:6]
The qRT-PCR confirmed changes of the selected miRNAs (Figure  4B), decreased expression of miR-96, miR-141, miR-182, miR-183, miR-200a, miR-200b, miR-429 and miR-451 in F2-SSS compared to F0-S animals, whereas miR-23b and miR-200c showed increased expression levels. [score:4]
In order to validate miRNAs, we performed quantitative real time PCR (qRT-PCR) analysis of these differentially regulated miRNAs (n = 3 per group for F0, F1 and F2 generations, three replicates per sample): miR-23b, miR-96, miR-141, miR-181a, miR-182, miR-183, miR-200a, miR-200b, miR-200c, miR429 and miR-451. [score:2]
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13
[+] score: 11
Our results indicated that miR-183 expression was significantly up-regulated at 3 d following CFA injection, whereas in the ipsilateral mandibular division of the TG, the level of miR-183 expression was reduced significantly within 4 h and then recovered to a normal level at 4 d after CFA injection into the rat masseter muscle [16]. [score:8]
In addition, spinal nerve ligation causes down-regulation of miR-183 at 2 weeks in the ipsilateral compared with the contralateral DRG [10]. [score:3]
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[+] score: 10
Other miRNAs from this paper: rno-mir-19b-1, rno-mir-19b-2, rno-mir-146b
An in vitro experiment showed that incubation of 3T3-L1 adipocytes with insulin results in a significant decrease in the miR-183-5p level (51); miR-183-5p can inhibit apoptosis in human hepatocellular carcinoma cells (52) and was found upregulated in cirrhotic liver and premalignant lesions (53). [score:6]
In the AP rats, miR-183-5p was upregulated in the PBMCs. [score:4]
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[+] score: 10
Clinically, miR-183 has been shown to be upregulated in whole blood samples from depressed patients on antidepressant treatment [42], highlighting that miR-183 is highly responsive to emotional stimuli. [score:4]
We demonstrated the presence of miRNAs that had a large fold increase (miR-3535, miR-673-5p) or decrease (miR-182-5p, miR-1964, miR-206-3p), that were normalized by colonization (miR-219a-2-3p (PFC), miR-182-5p, miR-183-5p (amygdala)) and that are known to be implicated in influencing anxiety levels and expression of neurotrophins such as brain-derived neurotrophic factor (BDNF) (miR-183-5p, miR-206-3p) [33, 34]. [score:3]
Specifically, miR-183 has been linked to regulating anxiety-related behaviours in the Indian field mouse through influencing acetylcholinesterase splicing [33]. [score:2]
Within the amygdala, we found that miR-183-5p and miR-182-5p were both decreased and subsequently normalized by colonization. [score:1]
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16
[+] score: 7
Hansen et al. found that the circular transcripts of SRY had 18 miR-183 binding sites and that CDR1as had 73 miR-7 binding sites [16], so they proposed scientific hypothesis and demonstrated that circRNA could function as miRNA sponges to regulate the expression of target genes indirectly. [score:7]
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[+] 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]
Intrathecal miR-183 delivery suppresses mechanical allodynia in mononeuropathic rats. [score:3]
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[+] score: 6
Few of the highly upregulated microRNAs were: miR-79, miR-183, miR-206, miR-207, miR-296-3p, miR-298, miR-380-5p, miR-433, miR-449b, miR-705, miR-761 (S1 Table). [score:4]
Majority of the dysregulated microRNAs e. g. miR-380, miR-207, miR-79, miR-129, miR-153, miR-183, etc. [score:2]
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[+] score: 5
Other miRNAs from this paper: rno-mir-200b, rno-mir-381, rno-mir-182
In contrast, the oncogenic miR-183/182/96 cluster of miRNAs is upregulated in a variety of tumours [9], [11], [12], and we previously reported that miR-183/182/96 cluster regulates oxidative apoptosis and sensitises gliomal cells to chemotherapy [13]. [score:5]
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[+] score: 5
MiR-21 blocked pancreatic β-cell death [28] and miR-183 suppressed apoptosis in esophageal cancer cells [29] by targeting PDCD4. [score:5]
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[+] score: 4
Other miRNAs from this paper: rno-mir-10a, rno-mir-30d, rno-mir-30a, rno-mir-96
Significant downregulation was observed for miR-96 and miR-183 in L5 DRG. [score:4]
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[+] score: 3
Among these aberrant miRNAs, ten miRs (miR-183-3p, miR-34c-3p, miR-200b, miR-466c, miR-465-3p, miR-185-3p, miR-320a, miR-493-5p, miR-181b-5p and miR-21-5p) were reported to be differentially expressed at both 12 and 48 h after IR. [score:3]
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[+] score: 3
We extracted 60 different human miRNAs that co-occur with this target gene from 79 PubMed abstracts, and some of them (e. g. hsa-let-7a, hsa-miR-30b, hsa-miR-183) are consistent with microarray -based results discussed by Shalgi et al. [44]. [score:3]
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[+] score: 3
MiR-183 also showed female-biased expression during middle age (Figure  7) and has been proposed as a promising biomarker for early detection and prognosis of certain cancers including colorectal and prostate [51]. [score:2]
Statistically significant sex differences were confirmed for miR-183, miR-204, and miR-142-3p (Figure  7B-D). [score:1]
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[+] score: 3
To confirm the deep sequencing results, we used qRT-PCR to assess the expressions of 10 of the miRNAs (miR-183-5p, miR-9a-5p, miR-199a-5p, miR-351-5p, miR200b-3p, miR-191a-3p, miR-181c-3p, miR-330-5p, miR-126a-5p and miR-351-3p) in the 12-pair plasma samples from the hyperoxia rats and controls. [score:3]
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[+] score: 2
Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-130a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-298, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, mmu-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-99b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-125a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-181c, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-572, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-193b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a, rno-mir-193b
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
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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: 2
For example, studies in mutant mice have shown that, miR-183/96/182 clusters and miR132/212 were essential for the synaptic development in retina [16- 18], and miR-124 was critical for the maturation of cone cells [19] in retina. [score:2]
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[+] score: 1
CRD-BP protects the coding region of betaTrCP1 mRNA from miR-183 -mediated degradation. [score:1]
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[+] score: 1
Inactivation of the microRNA-183/96/182 cluster results in syndromic retinal degeneration. [score:1]
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[+] score: 1
miR-182, of the miR-183 cluster family, is packaged in exosomes and is detected in human exosomes from serum, breast cells and prostate cells. [score:1]
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[+] score: 1
Among them, five miRNAs (let-7b, miR-1180, miR-183, miR-550b, and miR-133a) were only present in LPS pre-Exo. [score:1]
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[+] score: 1
On the other hand, mir-183 was affected by social enrichment in both brain regions, with its mature miR-183-5p showing a striking 300-fold decrease in the amygdala and 5-fold increase in the ventral striatum. [score:1]
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[+] score: 1
We selected the top 9 miRNAs (miR-200a, miR-200b, miR-182, miR-429, miR-183, miR-200c, miR-141, miR-96 and miR-24) showing the highest standard deviations. [score:1]
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[+] score: 1
Among the 24 specific miRNAs, 13 of them, such as miR-182/196a/381/499a/99a [6], miR-183 [6, 23], miR-409 [23], miR-146b [6, 24], miR-143 [6, 24], miR-148a [24, 25], miR-204 [5], and miR-9 [6], have been reported to involve in T2D process in mouse or rat. [score:1]
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