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15 publications mentioning rno-mir-186

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-186. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 209
Our results showed that the overexpression of miR-186-5p down-regulates FSHb expression and decreases FSH secretion in rat anterior pituitary cells, providing evidence that hormone secretion in the pituitary is regulated by miRNAs. [score:9]
FSHb expression and FSH secretion after the overexpression or inhibition of miR-186-5pWe further verified the interaction between miR-186-5p and FSHb in rat anterior pituitary cells and examined the role of this interaction in the regulation of animal reproduction. [score:8]
Taken together, our results showed that miR-186-5p down-regulates the expression of FSHb and inhibits the secretion of FSH. [score:8]
These results demonstrated that miR-186-5p can regulate FSHb by inhibiting the expression of FSHb and by decreasing the secretion of FSH via direct binding to the FSHb 3′ UTR. [score:7]
mRNA expression levels of FSHb and the level of FSH secretion after the overexpression or inhibition of miR-186-5p. [score:7]
We then examined the expression of miR-186-5p after transfecting cells with 100 nM miR-186-5p negative control, inhibitor negative control, mimic, and inhibitor. [score:7]
Since the over -expression and inhibition of miR-186-5p led to a significant reduction and increase in FSHb levels, respectively, we examined whether the same trends were observed for FSH secretion by ELISA after transfection for 24 h. FSH secretion and FSHb expression exhibited similar patterns in the four groups. [score:7]
0194300.g004 Fig 4mRNA expression levels of FSHb and the level of FSH secretion after the overexpression or inhibition of miR-186-5p. [score:7]
To further verify the interaction between miR-186-5p and FSHb, we predicted the target site of miR-186-5p in the FSHb 3′ UTR using TargetScan (Fig 1A), and mutated the target site TTCTTTA to AAGAAAT and ATTCTTT to TAAGAAA (Fig 1B). [score:7]
FSHb expression and FSH secretion after the overexpression or inhibition of miR-186-5p. [score:7]
In our previous study, miR-186-5p expression was significantly differentially expressed (0.45-fold difference) between the non-sexual maturity developmental stage and the sexual maturity developmental stage in the rat pituitary [16]. [score:7]
The overexpression of miR-186-5p significantly increased the expression of miR-186-5p (5653.605-fold, p < 0.01) compared with expression in the negative control group (Fig 3E). [score:6]
When we inhibited the expression of miR-186-5p, the level of miR-186-5p decreased (0.382-fold, p < 0.01) compared with levels in the inhibitor negative control group (Fig 3F). [score:6]
We detected miR-186-5p expression in 2-week- and 4-month-old rats to examine expression differences among developmental stages in the rat pituitary. [score:6]
miR-186-5p was expressed in all of these tissue types, and was particularly highly expressed in the lung, kidney, and brain (Fig 2B). [score:5]
In this study, the overexpression of miR-186-5p inhibited FSH secretion. [score:5]
FSHb expression levels were significantly higher in the miR-186-5p inhibitor group than in the I-NC group (1.29-fold, p < 0.05; Fig 4A). [score:5]
We detected miR-186-5p expression in both stages, and we found that compared with levels in the non-sexual maturity period, miR-186-5p was down-regulated in the sexual maturity period (Fig 2A). [score:5]
Specifically, rat primary pituitary cells were transfected using 100 nM negative control (NC), miR-186-5p mimic, inhibitor negative control (I-NC), and miR-186-5p inhibitor; after 24 h, the level of FSHb was examined by quantitative RT-PCR. [score:5]
Therefore, miR-186-5p and FSHb had a direct interaction, indicating that miR-186-5p could regulate FSHb expression. [score:5]
For quality control, we used flow cytometry to detect rat anterior pituitary cell apoptosis after transfection with 100 nM miR-186-5p negative control, inhibitor negative control, mimic, and inhibitor for 24 h. We did not detect significant differences among the negative control groups and transfection groups (Fig 3A–3D). [score:5]
In 2016, Huang et al. indicated that miR-186 suppresses cell proliferation and metastasis by targeting MAP3K2 in non-small cell lung cancer [35]. [score:5]
Accordingly, the over -expression or inhibition of miR-186-5p was successful. [score:5]
Detection of the differential expression of miR-186-5p at various developmental stages of the pituitary and in various tissues in rats. [score:4]
However, the increase in luciferase activity indicated that the predicted target sites were correct and miR-186-5p and FSHb had a direct interaction. [score:4]
Detection of differential miR-186-5p expression at various developmental stages in the pituitary and in other rat tissues. [score:4]
When E6/E7 is silenced, miR-186-5p is down-regulated in HPV18 -positive HeLa cells [38]. [score:4]
0194300.g002 Fig 2 (A) The relative expression level of miR-186-5p was detected in 2-week-old and 4-month-old rats, and U6 was used as an internal standard for qRT-PCR. [score:3]
However, in our study, when we co -transfected miR-186-5p mimics and pmiR-FSHb-3′UTR-WT into 293T cells, the luciferase activity was reduced by more than 40%; after mutating two target sites, luciferase activity was slightly higher, but still significantly different from wild-type levels. [score:3]
The inhibition of mir-186-5p significantly increased FSH secretion (6.02 ± 0.55 IU/L vs. [score:3]
We examined the expression of miR-186-5p in seven tissues of 4-month-old rats, including the pituitary, heart, liver, spleen, lung, kidney, and brain. [score:3]
In this study, to verify the interaction between FSHb mRNA and miR-186-5p, we mutated the target sites of miR-186-5p in the FSHb 3′ UTR. [score:3]
Moreover, in our study, miR-186-5p exhibited different degrees of expression in the rat heart, pituitary, liver, spleen, lung, kidney, and brain. [score:3]
The overexpression of miR-186-5p significantly decreased FSH secretion (6.19 ± 0.62 IU/L vs. [score:3]
Although miR-186-5p was not a tissue-specific miRNA in these rat tissues, its differential expression suggests that it is a candidate for further research. [score:3]
The miRNA miR-186-5p is an important tumor suppressor and has been observed in many types of human cancers, including gastric cancer, hepatocellular cancer, and glioblastoma multiforme [32– 34]. [score:3]
Two target sites of miR-186-5p and the FSHb 3′ UTR were mutated, i. e., TTCTTTA to AAGAAAT and ATTCTTT to TAAGAAA, to obtain pmiR-FSHb-3′UTR-MUT (S1 File). [score:3]
Accordingly, miR-186-5p is a potential regulator of pituitary development and reproduction. [score:3]
To determine whether miR-186-5p regulates FSH secretion, we measured the mRNA expression levels of FSHb and the secretion of the FSH hormone after the transfection of miR-186-5p into primary rat pituitary cells. [score:2]
We further verified the interaction between miR-186-5p and FSHb in rat anterior pituitary cells and examined the role of this interaction in the regulation of animal reproduction. [score:2]
MiR-186-5p targets the 3′ UTR of FSHb mRNA. [score:2]
FSHb mRNA levels decreased significantly (0.66-fold, p < 0.05; Fig 4A) after the overexpression of miR-186-5p compared with the levels in the NC group. [score:2]
MiR-186-5p targets the 3′ UTR of FSHb mRNAIn our previous study, a luciferase reporter assay indicated that miR-186-5p mimics reduce luciferase activity by 32% compared with that of a negative control group [16]. [score:1]
Next, we constructed pmiR-FSHb-3′UTR-MUT and co -transfected miR-186-5p mimics and pmiR-FSHb-3′UTR-MUT into 293T cells. [score:1]
Effect of miR-186-5p transfection into rat primary pituitary cells. [score:1]
These studies demonstrated that miR-186-5p acts as an anti-oncogenic marker and is involved in the control of cell proliferation, senescence, and apoptosis. [score:1]
In addition, in nonmelanoma skin cancer, miR-186-5p could be a novel noninvasive biomarker for detection [36]. [score:1]
Despite a number of studies indicating that miR-186-5p is associated with human cancers, its role in hormone secretion is unclear. [score:1]
The seven tissues were used to measure the expression of miR-186-5p in different tissues. [score:1]
Thananya et al. showed that miR-186-5p might be a specific hepatic miRNA that responds to hepatitis B virus and predicts the response to pegylated-interferon alpha-2a [37]. [score:1]
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2
[+] score: 87
Other miRNAs from this paper: rno-mir-381, rno-mir-709
Two miRNAs, miR-186 and miR-381, were up-regulated, while miR-709 was down-regulated. [score:7]
We confirmed the expression of several mRNA and miRNAs and demonstrate that miR-186 targets Eps15. [score:5]
Computational analysis of predicted targets for miR-186 revealed 365 putative miRNA targets, with a total of 398 conserved sites and 271 poorly conserved sites, with the score from −1.31 (most favorable) to 0.00 (data are not shown). [score:5]
We have found that for the efficient regulation of a target gene (Eps15) the seed sequence miR-186 can have one mismatch. [score:4]
We did not observe any significant changes for miR-186 in stress and control animals after two weeks of stress, however, miRNA-186 was significantly up-regulated in cerebellum after two weeks of recovery from stress (Fig. 9A). [score:4]
A: Dose -dependent inhibition of Eps15 expression in the Luciferase Assay after transfection of HEK-293 cells with miR-186. [score:4]
0029441.g010 Figure 10A: Dose -dependent inhibition of Eps15 expression in the Luciferase Assay after transfection of HEK-293 cells with miR-186. [score:4]
miR-186 showed similar expression patterns in hippocampus and prefrontal cortex (Fig. 9C and E). [score:3]
Table S10 data of miR-186 expression in prefrontal cortex. [score:3]
We performed analysis to confirm changes in miR-186 and miR-709 expression after two weeks of stress, and to investigate their expression after four weeks. [score:3]
The 3′- untranslated regions (UTR) of the Eps15 gene (NM_001009424) with a seed sequence for the miR-186 and Nab1 (NM_022856) genes with a binding site for miR-709 (see Fig. S5) were amplified by PCR. [score:3]
Currently there are no confirmed targets for miR-186 and miR-709 in the brain. [score:3]
analysis of miR-186 (A,C,E) and miR-709 (B,D,F) expression level in cerebellum (A,B), hippocampus (C,D), and prefrontal cortex (E,F). [score:3]
confirmed the expression of miR-186 and miR-709. [score:3]
Table S6 data of miR-186 expression in cerebellum. [score:3]
miR-186 was reported to be expressed by postnatal oligodendrocyte lineage cells [55]. [score:3]
Figure S3 data of miR-186 expression. [score:3]
Our study revealed that miR-186 can target Eps15 in mammalian cells. [score:3]
Changes in miR-186 expression. [score:3]
In particular, miR-186 and miR-709, which changed significantly in response to stress, do not belong to those which are abundantly expressed in the brain, and particularly in the cerebellum. [score:3]
Table S8 data of miR-186 expression in hippocampus. [score:3]
Thus, miR-186 and miR-709 may trigger a cascade of molecular reactions which are important in the regulation of the stress response. [score:2]
Analysis of Luciferase Assay data showed that the luciferase activity was inhibited by miR-186 after co-transfection of mammalian cells with the construct carrying Eps-15 3′UTR in a dose -dependent manner (Fig. 10A). [score:2]
To confirm that Eps15 is indeed targeted by miR-186 we carried out a luciferase reporter assay. [score:2]
Figure S5A: Putative binding site of mir-186 in Eps15 3′UTR. [score:1]
Third bar: pFN4 mut + miR-186. [score:1]
For further analysis only miRNAs with the lowest p-value (p<0.01) were used, which included miR-186 (log [2] ratio of 0.43) and miR-709 (log [2] ratio of −0.66). [score:1]
Second bar: pFN4 + miR-186. [score:1]
The miR-186 binding sequence (highlighted in red) was substituted with the mutated sequence (adenine was substituted by guanine, while thymine was substituted by guanine). [score:1]
The 3′UTR of the Eps15 gene (NM_001009424) contains one binding site with a poorly conserved sequence for rno-miR-186 with one mismatch. [score:1]
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3
[+] score: 16
stress also downregulated miR-186 in the maternal frontal cortex, which is in contrast to the upregulation found in frontal cortex, hippocampus, and cerebellum in male rats [25]. [score:7]
Note that prenatal stress downregulated miR-181 and miR-186 expression in the frontal cortex. [score:6]
Stress also led to critical decreases in let-7c, miR-23b, miR-181, and miR186 amounts. [score:1]
miR-181 and miR-186 were chosen for verification using qRT-PCR analysis. [score:1]
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]
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4
[+] score: 10
Other miRNAs from this paper: rno-mir-328a, rno-mir-328b
There are many factors involved in the regulation of myogenin gene expression, such as HuR, Twist, CACNb1, miR-186 and miR-328 [25– 28, 32]. [score:4]
Twist, HuR and miR-186 are not involved in the effect of DXR on myogenin expression. [score:3]
MiR-186, HuR and CACNb1 may mediate myogenin expression through different pathways [26– 28]. [score:2]
Unfortunately, we did not identify miR-186. [score:1]
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5
[+] score: 9
We then used a screening system based on the luciferase reporter plasmid carrying the full-length 3′UTR of the FSHb mRNA and found that 18 miRNAs, specifically miR-433-3p, miR-323-3p, miR-328a-3p, miR-3573-3p, miR-204-5p, miR-206-5p, miR-31a-5p, miR-7a-5p, miR-880-3p, miR-186-5p, miR-503-5p, miR-383-5p, miR-324-5p, miR-505-5p, miR-27b-3p, miR-221-5p, miR-320-3p and miR-21-3p, could suppress the expression of the reporter by more than 30% (Figure 1). [score:5]
Interestingly, we identified 12 other miRNAs (miR-323-3p, miR-328a-3p, miR-3573-3p, miR-204-5p, miR-206-5p, miR-31a-5p, miR-7a-5p, miR-880-3p, miR-186-5p, miR-503-5p, miR-383-5p and miR-320-3p) that might also regulate FSHb expression, and then affected FSH secretion, but their specific effects need to be verified through further experiments. [score:4]
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6
[+] score: 4
MicroRNAs like miR-19a, 34b, 129, 135a, 142-3p, miR-153, miR-186, miR-187, and miR-301a were significantly downregulated in Cs1-ko mice. [score:4]
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7
[+] score: 3
miR-186, miR-216b, miR-337-3p, and miR-760 cooperatively induce cellular senescence by targeting α subunit of protein kinase CKII in human colorectal cancer cells. [score:3]
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8
[+] score: 3
Some miRNAs such as miR-24, miR-186, let-7f and miR-320 showed changes in expression throughout all time points (Figure S2C). [score:3]
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9
[+] score: 3
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Another subgroup of miRNAs displayed an opposite pattern, i. e. decreased expression during latency: miR-7a-1-3p, miR-107-3p, miR-138-5p, miR-139-3p, miR-186-5p, miR-204-5p, miR-222-3p, miR-324-3p and miR-505-3p were significantly decreased during latency (peak at 4 days after SE), then gradually returned to control levels (Fig. 2, Supplementary Fig. S2). [score:3]
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10
[+] score: 2
Hypoxia reduced the level of miR-186 at the first time point (1 day) and this change persisted and reached significance after 5 days of exposure to hypoxia with a 40% reduction. [score:1]
Hypoxia reduced the level of miR-186 after 1-day exposure and this change persisted and reached significance after 5 days of exposure to hypoxia. [score:1]
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11
[+] score: 1
Therefore, we began this study with myocardin as the focus molecule and profiled four selected miRNAs, including miR-1, miR-9, miR-128 and miR-186 which were predicted by miRanda (http://www. [score:1]
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12
[+] score: 1
173 (miR-186-5p, miR-208a-5p, miR-291a-3p, miR-294-3p, miR-295-3p, miR-302a-3p, miR-302b-3p, miR-302c-3p and miR-302d-3p). [score:1]
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13
[+] score: 1
A number of other miRNA species that might affect collagen type-I and -IV synthesis, such as miR-106a/b, miR-20a/b, miR-26a/b, miR-374a/b, miR-186 were also identified by in silico analyses (summarized in Table 1). [score:1]
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14
[+] score: 1
At late-stage diabetes, the circulating level of 12 miRNAs was specifically altered; the circulating level of miR-375, miR-210 and miR-133a was increased, and the circulating levels of let-7i, miR-140, miR-450a, miR-185, miR-186, miR-151-3p, miR-203, miR-16 and miR-685 were strongly diminished versus their levels at the pre-diabetes stage (Figure 4). [score:1]
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15
[+] score: 1
Both miR-29a and miR-186 are some of the most frequently detected miRNAs in plasma and serum [46]. [score:1]
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