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25 publications mentioning rno-mir-96

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-96. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 153
Other miRNAs from this paper: rno-mir-34a, rno-mir-146a
A target prediction performed with the miRWalk database and other programs (miRanda, Sanger miRDB, RNAhybrid and Targetscan) predicted both Atg7 and Atg16L1 to be direct targets of miR-96. [score:8]
As shown in Fig.   6A and B, overexpression of miR-96 significantly inhibited Atg7 and Atg16L1 expression in the hippocampus of SE rats. [score:7]
Overexpression of miR-96 significantly prevents SE rats from brain damage by inhibiting the Atg7 and Atg16L1 expression and consequently, autophagosome formation in the hippocampus. [score:7]
Overexpression of miR-96 through intracerebral injection had a preventive role on SE -induced brain damage, by inhibiting Atg7 and Atg16L1 expression, followed by autophagosome formation in immature rats. [score:7]
The target prediction indicated that Atg7 and Atg16L1 were both direct targets of miR-96. [score:6]
Furthermore, our results indicated that a reduction of miR-96 was inversely correlated with the up-regulation of Atg7 and Atg16L1 expression. [score:6]
As shown in Fig.   8A,B, Rapamycin attenuated miR-96 mediated reduction in the ratio of LC3II/LC3I and upregulation of p62 expression (Fig.   8A,B). [score:6]
results indicated a dramatic up-regulation of miR-96 expression in the miR-96 mimics injection group (Fig.   5B). [score:6]
Pearson correlation analysis demonstrated that miR-96 expression was inversely correlated with Atg7 (r = −0.85, p = 0.001, Fig.   4C) and Atg16L1 (r = −0.93, p = 0.001, Fig.   4D) expression in the hippocampus of rats with SE. [score:5]
miR-96 inhibits expression of Atg7 and Atg16L1 in the hippocampus of SE rats. [score:5]
Pearson correlation analysis revealed that miR-96 expression was inversely correlated with Atg7 (r = −0.85, p = 0.001) and Atg16L1 (r = -0.93, p = 0.001) expression in the hippocampus of rats with SE (Fig.   4E). [score:5]
Furthermore, injection of miR-96 mimics significantly prevented SE rats from brain damage (Fig.   5) by inhibiting Atg7 and Atg16L1 expression (Fig.   6) and autophagosome formation (Fig.   7) in the hippocampus. [score:5]
Taken together, these results show that injection of miR-96 significantly inhibited the expression of Atg7 and Atg16L1 in the hippocampus. [score:5]
To further elucidate the molecular mechanism underlying the protective role of miR-96 in SE -induced brain injury, we qualified the expression of miR-96 predicted targets Atg7 and Atg16L1 by immunofluorescence staining and Western blot analysis. [score:5]
In our previous study [23], an miRNA array and related bioinformatics analysis by KEGG analysis 27– 29 indicated that miR-96 was one of the miRNAs with significantly altered expression and that the autophagy signalling pathway was regulated by these de-regulated miRNAs underlying epileptogenesis (Fig.   4A). [score:5]
Western blot analysis also showed a 64.4% reduction in the ratio of LCII/LC3I and a 3.8 fold upregulation of p62 expression in the miR-96 mimics -injected hippocampus, when compared to the negative control (Fig.   7B). [score:5]
Our study suggests that miR-96 gets its protective role during the development of SE, thus providing a novel therapy target for SE therapy. [score:4]
Figure 4Downregulation of autophagy-related miR-96 in the hippocampus of SE rats. [score:4]
Down-regulation of autophagy-related miR-96 in the hippocampus of SE rats. [score:4]
Our study also suggests that miR-96 acquires its protective role during the development of SE, thereby supporting its role as a novel therapeutic target for SE. [score:4]
The clear down-regulation of Atg7 and Atg16L1 expression in the miR-96 -injected hippocampus motivated us to investigate changes in autophagosome formation in the groups submitted to the different treatments. [score:4]
miR-96 is one of the miRNAs showing significantly differential expression and correlated with the autophagy signalling pathway [23]. [score:3]
In conclusion, injection of miR-96 could inhibit autophagosome formation in the hippocampus. [score:3]
miR-96 inhibits hippocampus autophagosome formation in SE rats. [score:3]
Figure 5Overexpression of miR-96 attenuates SE -induced brain injury. [score:3]
After normalisation to β-actin expression, we found a 59.4% decrease in Atg7 and a 66.7% decrease in Atg16L1 protein levels (Fig.   6C) in the miR-96 -injected hippocampus. [score:3]
This suggests that miR-96 might be a potential target for therapy of pediatric SE. [score:3]
In conclusion, our study is the first to demonstrate an increase in autophagosomes in neurons after SE, accompanied by the induction of Atg7 and Atg16L1 expression, which result from a reduction in miR-96 levels. [score:3]
Overexpression of miR-96 attenuates SE -induced brain injury. [score:3]
To further validate the expression of miR-96, total mRNA was isolated from the hippocampus of SE rats at 2, 6, 12, 24, 48, 72 and 144 h post insult and used for a quantitative reverse transcription polymerase chain reaction (qRT-PCR) assay. [score:2]
Furthermore, HE staining and Nissl staining demonstrated that there were no significant difference on disorganized cells and Nissl bodies between SE-Rapamycin-miR-NC injection group and SE-Rapamycin-miR-96 mimics injection group (Fig.   8C,D). [score:1]
In the present study, we further investigated the potential autophagy-related miR-96, which we propose can be used as a diagnostic and therapeutic target for SE in immature rats. [score:1]
To further elucidate the autophagy effects underlying the protective role of miR-96 in SE -induced brain injury, we employed Rapamycin to treat miR-NC or miR-96-mimcs injected SE rats. [score:1]
Rapamycin negated miR-96 mediated brain injury attenuation. [score:1]
In the miR-96 injection group, only 8.5% and 10.4% cells were Atg7- and Atg16L1-immunoreactive, respectively (Fig.   6(A,B)). [score:1]
Figure 8Rapamycin negated miR-96 mediated brain injury attenuation. [score:1]
These results indicate that injection of miR-96 mimics significantly prevents brain damage in SE rats. [score:1]
To validate the potential protective role of miR-96 in SE -induced brain injury, miR-96 mimics were intracerebrally injected. [score:1]
indicated that less LC3 -positive cells were found in the miR-96 -injected hippocampus, a 73.4% decrease (Fig.   7A). [score:1]
Therefore, to our knowledge, our study is the first to show miRNA (miR-96) to be involved in autophagy during epileptogenesis. [score:1]
As shown in Fig.   5A, 10 nmol miR-96 mimics or miR negative control (miR-NC), diluted in 5 μl phosphate buffer saline (PBS), were injected into the right cerebral hemisphere of SE rats using a 30-gauge needle with a 5 μl Hamilton syringe, 4 h prior to the SE insult. [score:1]
However, in the SE-miR-96 mimics injection group, the number of disorganized cells in the CA1 and CA3 areas was greatly reduced (Fig.   5C). [score:1]
miR-96 mimics and negative control (NC) were purchased from Ribobio (Guangzhou, China) and 10 nmol miR-96 mimics or NC in 5 μl PBS was injected into the right cerebral hemisphere of SE insult rats using a 30-gauge needle with a 5-μl Hamilton syringe injections. [score:1]
The results indicated that miR-96 levels decreased from 2 to 72 h after SE and returned to basal levels after 144 h (Fig.   4B). [score:1]
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2
[+] score: 105
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-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-183, 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 (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]
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, 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]
Interestingly, the expression of miRNA-96 is up-regulated in response to ACTH treatment, but is down-regulated following DEX treatment. [score:9]
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]
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]
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]
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]
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]
Real-time PCR (qRT-PCR) confirmed ACTH -mediated up-regulation of miRNA-212, miRNA-183, miRNA-182, miRNA-132 and miRNA-96. [score:4]
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]
The expression levels of miRNA-122 and miRNA-96, however, were not affected by cAMP stimulation. [score:3]
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]
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]
Those miRNAs differentially expressed on the microarrays with greatest fold changes, miRNA-101a, miRNA-142-3p, miRNA-433 and miRNA-96, were further analyzed. [score:3]
Furthermore, such DEX alteration of adrenal miRNA levels demonstrates that DEX suppression of endogenous ACTH secretion modulates a set of adrenal miRNAs, with the exception of miRNA-96, miRNA-466, and miRNA-27a, that are distinct from those modulated by treatment with exogenous ACTH. [score:3]
MiR-183, miR-96 and miR-19a were predicted to target the ABCA1 gene. [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]
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]
[1 to 20 of 20 sentences]
3
[+] score: 29
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]
Intrathecal miR-96 inhibits Nav1.3 expression and alleviates neuropathic pain in rat following chronic construction injury. [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]
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]
In particular, miR-96 was also involved in CCI mo del (Chen et al., 2014). [score:1]
[1 to 20 of 7 sentences]
4
[+] score: 28
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-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-183, 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
Accordingly, expression of miR-96 in PCOS shows a 6-fold down-regulation compared to control ovary and is localized in the theca and cumulus-granulosa of cystic follicles. [score:5]
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]
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]
For example, rno-miR-96, rno-miR-31 and rno-miR-222 were exclusively expressed in the theca of cystic follicles. [score:3]
FOXO3a, a target of miR-96, promotes cancer cell proliferation [55]. [score:3]
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]
Thus, the cell proliferation in the preantral follicles in hyperandrogenic condition could be induced through a mechanism utilizing miR-96 -mediated regulation. [score:2]
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]
[1 to 20 of 9 sentences]
5
[+] score: 27
Despite only seven sexually dimorphic miRNAs being in common between the adult and the old rats (miR-125b-5p, miR-152, miR-29b, miR-374, miR-96, miR-99a*, and miR-99a), 91% (74/81) of the mRNA targets in the old rats were also mRNA targets in the adult rats. [score:5]
miR-221 and miR-96 showed relatively larger sex differences over the middle portion of the life span, with miR-221 expressed at 3-to 14.3-fold higher levels in males than females from 8 to 21 weeks of age, and miR-96 expressed at 2.2 to 7.2 higher levels in males than females from 21 to 78 weeks of age. [score:5]
The average log2 relative expression per group of qPCR and microarray data are displayed for miR-29b, miR-34a, miR-96, and miR-154* such that the global average expression for qPCR (n = 5) and microarray data (n = 4 or 5) is equal to zero. [score:5]
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]
Taqman qPCR results confirmed this male-biased miR-96 expression at 78 weeks of age and additionally at 104 weeks of age (Fig.   6b). [score:3]
Microarray data for miR-96 showed male-biased expression at 21, 52, and 78 weeks of age. [score:3]
[1 to 20 of 7 sentences]
6
[+] score: 26
In contrast, miR-200a-3p expression, and potentially the expression of all miRNAs specified by the three clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429, tend to be up-regulated with similar FCEs in both experimental conditions. [score:8]
Co-variation of miRNA expression also demonstrated that the transcription and maturation of clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429 are co-regulated in ARC. [score:4]
Altogether our new and previous findings point to a trend to the long-term overexpression of clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429 in the ARC of adult rats and mice having experienced low levels of leptin/leptin signaling during the perinatal period. [score:3]
miR-96 regulates the progression of differentiation in mammalian cochlear inner and outer hair cells. [score:2]
Punctual mutation or deletion in cluster miR-96/182/183 produces ear or retina disorders while loss of function of the miR-200 family leads to defects in the terminal differentiation of olfactory precursors (Choi et al., 2008; Kuhn et al., 2011; Lumayag et al., 2013). [score:2]
The specific case of clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429. [score:1]
Among those miRNAs were all the 10 miRNAs produced from miR gene clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429. [score:1]
In these groups, miRNAs produced from clusters miR-96/182/183, miR-141/200c, miR-200a/200b/429 also appeared as hypervariable miRNAs (see Table 2). [score:1]
Ten miRNAs are produced by clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429. [score:1]
miRNAs specified by clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429 have been identified as miRNAs of functional importance in sensory organs. [score:1]
Among the 15 (3.6%) miRNAs displaying MAX/MINs larger than this value, 8 were produced from three miR gene clusters, namely the miR-96/182/183 cluster and the two evolutionary-related clusters miR-141/200c and miR-200a/200b/429 (Table 2). [score:1]
Figure 5 The specific case of the miRNAs specified by clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429. [score:1]
[1 to 20 of 12 sentences]
7
[+] score: 18
For instance, the up-expressed miR-143 and miR-138 can, respectively, target the genes, HK2 and HK1, which are the crucial enzymes in glycolysis and so that lead to potential glycemia [28, 29]; miR-9 and miR-204 were reported that they can regulate the insulin secretion by targeting the gene, SIRT1 [30– 32], while miR-96 can decrease the expression of NOC2 which is involved in the insulin secretion [33]. [score:10]
From the previous study, the miR-96/182/183 cluster is regulated by SREBP-2 which is a function as it activates the expression of many key genes for cholesterol level and uptake. [score:4]
From Table 1, as the cholesterol level was even higher in T2D than healthy individuals, the miR-96/182/183 would accordingly come to be downexpressed [34]. [score:3]
The miR-381-3p, miR-548u, miR-411-5p, miR-148a-5p, and miR-96-5p which were filtered in HFD comparison but not in intact comparison and no-T2D comparison might involve the progress of T2D fed with HFD only. [score:1]
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8
[+] 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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9
[+] score: 8
This would likely be the case for the observed increases in the expression of the cell death inducers caspase 3 [69], [70] and Fas [71], the expression of which parallels the decreased expression of their regulators, the let7/miR-98 family members miR-96 and miR-146a. [score:8]
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10
[+] score: 7
Other miRNAs from this paper: rno-mir-10a, rno-mir-30d, rno-mir-30a, rno-mir-183
Significant downregulation was observed for miR-96 and miR-183 in L5 DRG. [score:4]
A recent study, performed 2 weeks after SNL, focused on three miRNAs that are expressed as a cluster (miR-96, -182, and -183) in L5 DRG [52]. [score:3]
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11
[+] score: 6
Other miRNAs from this paper: rno-mir-34a, cgr-mir-34a
Accordingly, MC-LR has been shown to induce sperm abnormalities by downregulating miR-96 and altering deleted-in azoospermia -associated protein 2 (DAZAP2) expressions [12]. [score:6]
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12
[+] score: 5
Other miRNAs directly regulating insulin secretion affecting the expression of proteins involved in the exocytotic process include miR-124a and miR-96 [21]. [score:5]
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13
[+] score: 5
Other miRNAs from this paper: rno-mir-93, rno-mir-143, rno-mir-206, rno-mir-155
Intrathecal miR-96 inhibits Nav1.3 expression and alleviates neuropathic pain in rat following chronic construction injury. [score:5]
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14
[+] score: 4
In 2009, Aldrich et al. showed for the first time a downregulation of miR-96, -182 and -183 in DRG of rats in the context of neuropathic pain [16]. [score:4]
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15
[+] score: 4
Molecular basis of differential target regulation by miR-96 and miR-182: the Glypican-3 as a mo del. [score:4]
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16
[+] score: 4
Other miRNAs from this paper: rno-mir-21, rno-mir-152, rno-mir-193a, rno-mir-210, rno-mir-193b
Previous studies showed that expression of four miRNAs, including miR-96, miR-193-3p, miR-210, and miR-21, were correlated with the skin flap mo del in rat [9]. [score:3]
In Figure 1G, the results of laser Doppler velocimetry showed that relatively low blood flow in Part C. Positive correlation between ischemia-reperfusion injury in the skin flap of rat and four miRNAs (miR-21, miR-96, miR-193, and miR-210) has been demonstrated in previous studies [9]. [score:1]
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17
[+] score: 3
Other miRNAs from this paper: rno-mir-26a
Kinoshita C. Aoyama K. Matsumura N. Kikuchi-Utsumi K. Watabe M. Nakaki T. Rhythmic oscillations of the microRNA miR-96-5p play a neuroprotective role by indirectly regulating glutathione levelsNat. [score:3]
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18
[+] score: 3
For example, mutation in the seed region of miR-184 causes familial keratoconus with cataract [14] and mutations in the seed region of miR-96 are responsible for nonsyndromic progressive hearing loss [15]. [score:3]
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19
[+] score: 3
Most of the miRNAs in Fig.   4 were also highly expressed in the serum of normal adolescent rats, with the exception of mir-96, miR-96-5p, and miR-150-3p. [score:3]
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20
[+] score: 3
Some of the diabetes -associated miRNAs were below the detection limit in our study, such as miR-9, miR-96 and miR-148, indicating that back-translation from humans to ZDF rats may be difficult for these markers. [score:3]
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21
[+] score: 2
Guttilla et al. have shown that FOXO1 can be coordinately regulated by miR-27a, miR-96, and miR-182 38. [score:2]
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22
[+] score: 2
We noted that miRNAs miR-34a, miR-18a, miR-19a, miR-32, miR-96, miR-142-3p miR-29b and miR-7b were significantly upregulated in the AOM rat fecal colonocytes compared to those obtained from the saline controls and the degree of induction was greater in the tumor bearing AOM rats compared to the tumor non-bearing AOM rats (Fig. 3B). [score:2]
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23
[+] score: 1
Old age -associated miRNAs showed enrichment in pathways related to endocrine system disorders (miR-129-1, miR-375, miR-223, miR-664, miR-29b, miR-34a), cancer (miR-223, miR-29b, miR-375, miR-96), and cellular movement/invasion of cells (miR-29b, miR-29c, miR-7a, miR-96, miR-34a, miR-375). [score:1]
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24
[+] 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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25
[+] score: 1
When ER stress reaches a certain threshold, IRE1α selectively degrades four pre-microRNAs, including four microRNAs (miR-17, miR-34a, miR-96 and miR-125b) [49]. [score:1]
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