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6 publications mentioning rno-mir-487b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-487b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 231
By suppressing caspase-3 activity and enhancing the expression of the inhibitor of apoptosis (IAP) family of proteins, IL-33 reduces fibrosis and cardiomyocyte apoptosis and improves ventricular function, whereas the elevated sST2 expression inhibits IL-33 function, but miR-487b promotes the protective response of IL-33 in the heart because it binds to the IL-33 3’-untranslated region to activate IL-33 transcripts [24, 26]. [score:13]
The rats were divided into 10 groups (8 rats of each group): the blank group (treated with nothing), the sham group (coronary artery occlusion without ligation operation), the CHF group (construction of the CHF rat mo del), the miR-487b mimic group (tail vein injection of miR-487b mimic after one-week adaptive experiment), miR-487b inhibitor group (tail vein injection of miR-487b inhibitor), the negative control (NC) group (including NC of si-IL-33, NC of miR-487b mimic, and NC of miR-487b inhibitor; tail vein injection of nonsense sequence), the si IL-33 group (tail vein injection of IL-33 siRNA sequence), and the miR-487b inhibitor + si IL-33 group (transfection of miR-487b inhibitor and IL-33 siRNA sequence). [score:11]
We synthesized the overexpressed subject of miR-487b (miR-487b mimic) and the inhibitor of miR-487b (miR-487b inhibitor) and suppressed the expression subject of IL33 (si IL-33). [score:11]
Compared with the CHF group, IL-33 and ST2 mRNA expression decreased in the miR-487b mimic and si IL-33 groups, whereas miR-487b expression in the miR-487b mimic group was higher than that in the CHF group (P < 0.05 for all), and IL-33 and ST2 mRNA expression increased, whereas miR-487b expression decreased in the miR-487b inhibitor group (P < 0.05 for all) (Figure 7). [score:10]
We found that the miR-487b mimic group showed downregulated IL-33 and ST2 as well as upregulated miR-487b, and less cell apoptosis, inflammatory responses of myocarditis, and fibrosis were observed in this group, suggesting miR-487b alleviates CHF through inhibition of the IL-33 and ST2 signaling pathway. [score:9]
Expression in each group increased compared with expression in the blank and sham groups (P < 0.05 for all), and expression in the si IL-33 and miR-487b mimic groups were lower than in the CHF group but higher than in the blank and sham groups (P < 0.05 for all), and expression in the miR-487b inhibitor group increased compared with the CHF group (P < 0.05 for both). [score:9]
Yamazumi et al [32] reported that miR-487b was negatively correlated with the expression IL-33, and because expression of IL-33 and ST2 showed the same changing direction in CHF patients, it is plausible that miR-487b also inhibits ST2 [13, 29]. [score:8]
The results of qRT-PCR showed that when compared with the blank and sham groups, IL-33 and ST2 mRNA expression increased, whereas miR-487b expression decreased in the CHF, NC of miR-487b mimic, NC of miR-487b inhibitor, NC of si-IL-33, and miR-487b inhibitor + si IL-33 groups (P < 0.05 for all). [score:8]
There were no differences among the mRNA and protein expressions of IL-6 and TNF-α in the NC of miR-487b mimic, NC of miR-487b inhibitor, NC of si IL-33, miR-487b inhibitor + si IL-33, and CHF groups (P > 0.05 for all) (Figure 6). [score:7]
In vivo transfection and groupingDNA oligonucleotides of overexpressed and low-expressed RNA of miR-487b were synthesized to activate the sequence that effectively promotes miR-487b expression, and later DNA oligonucleotides were made into double-stranded DNA, followed by connection and transformation with pGCSIL-GFP vector digested by Age I and EcoR I for screening positive clones by polymerase chain reaction (PCR), and plasmid was extracted, digested, and sequenced. [score:7]
MiRNAs, including miR-487b, can function as posttranscriptional inhibitors, and in the context of inflammation they inhibit the production of cytokines such as IL-6 and TNF-α by repressing gene transcription, preventing translation, and destabilizing mRNA [18]. [score:7]
In this context, we explored new therapeutic approaches for CHF through discussing miR-487b suppression of IL-33 to inhibit the IL-33/ST2 signaling pathway in that disease. [score:7]
Endogenous small, noncoding miRNAs can stimulate gene expression via acceleration of mRNA activation or prevent translation through imperfect sequence-specific interaction with the 30-untranslated region of mRNAs, among which miR-487b is encoded by the 14q32.31 locus [8, 9]. [score:7]
DNA oligonucleotides of overexpressed and low-expressed RNA of miR-487b were synthesized to activate the sequence that effectively promotes miR-487b expression, and later DNA oligonucleotides were made into double-stranded DNA, followed by connection and transformation with pGCSIL-GFP vector digested by Age I and EcoR I for screening positive clones by polymerase chain reaction (PCR), and plasmid was extracted, digested, and sequenced. [score:7]
As shown in Figure 8, compared with the blank and sham groups, ST2 and IL-33 protein expression increased in the CHF, NC of miR-487b mimic, NC of miR-487b inhibitor, NC of si IL-33, and miR-487b inhibitor + si IL-33 groups (P < 0.05 for all) but decreased in the miR-487b mimic group and the si IL-33 group (P < 0.05 for all). [score:6]
The number in the miR-487b inhibitor group increased compared with the CHF group (P < 0.05), and there were no significant differences in the NC of miR-487b mimic, NC of miR-487b inhibitor, NC of si IL-33, and miR-487b inhibitor + si IL-33, and CHF groups (P > 0.05 for all) (Figure 5). [score:6]
Our data demonstrated that miR-487b ameliorates cell apoptosis, inflammatory reaction of myocarditis, and fibrosis through inhibiting the IL-33/ST2 pathway by suppressing IL-33, providing a novel therapy for CHF. [score:5]
MDA content and SOD activity were not significantly different in the NC of miR-487b mimic, NC of miR-487b inhibitor, NC of si IL-33, miR-487b inhibitor + si IL-33, and CHF groups (P > 0.05 for all) (Table 5). [score:5]
In the CHF, NC of miR-487b mimic, NC of miR-487b inhibitor, NC of si-IL-33, and miR-487b inhibitor + si IL-33 groups, the myocardial cells had hypertrophy and many green collagen fibers, were decreased in number, and were disorderly arranged in the intercellular space. [score:5]
As shown in Tables 3 and 4, the HW/BW and LVW/BW were higher in the CHF, NC of miR-487b mimic, NC of miR-487b inhibitor, NC of si-IL-33, and miR-487b inhibitor + si IL-33 groups than those in the blank and sham groups (P < 0.05 for all). [score:5]
Comparisons of miR-487b expression and mRNA expressions of IL-33/ST2 signaling pathway -associated proteins of rats among eight groups. [score:5]
There were no significant differences in cardiac function in the blank, sham, CHF, NC of miR-487b mimic, NC of miR-487b inhibitor, NC of si IL-33, and miR-487b inhibitor + si IL-33 groups (P > 0.05 for all). [score:5]
After the successful construction of the CHF mo del, caudal vein injection was conducted in the rats to transfect a sequence in the miR-487b mimic, control, NC of si-IL-33, NC of miR-487b mimic, NC of miR-487b inhibitor, si-IL-33, and miR-487b inhibitor + si-IL-33 groups, repeated every 3 days. [score:5]
DCM: dilated cardiomyopathy; IL-33/ST2: interleukin-33/somatostatin 2; IL-33: interleukin-33; sST2: somatostatin 2. qRT-PCR was performed to detect the expression of mir-487b in myocardial tissue of rat in each group, which demonstrated that the expression of miR-487b decreased in the CHF group compared with the blank and sham groups (P < 0.05, for both; Figure 2). [score:4]
Protein expression was higher than in the miR-487b inhibitor group compared with the CHF group (P < 0.05 for all). [score:4]
Moreover, downregulation of miR-487b increases invasion, tumorigenicity and proliferation of cells. [score:4]
Effects of miR-487b expression in myocardial tissues of the blank, sham, and CHF groups. [score:3]
Comparisons of expressions of IL-33, sST2, miR-487b, IL-6, and TNF-α between the CHF group and the control group. [score:3]
Figure 1Comparisons of expressions of IL-33, sST2 (A) IL-6, and TNF-α (B) and miR-487b (C) between the CHF and control groups. [score:3]
Figure 7The mRNA and expressions of miR-487b (A) and IL-33/ST2 signaling pathway -associated proteins (B) in rat myocardial tissues of eight groups. [score:3]
Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression of miR-487b, IL-33, ST2, IL-6, and TNF-α mRNA in right ventricular myocardial tissues in each group. [score:3]
This study investigated the effects of miR-487b activation of IL-33 through inhibition of the IL-33/ST2 signaling pathway in CHF, and we found that miR-487b suppresses the apoptosis, the inflammatory reaction of myocarditis, and myocardial fibrosis. [score:3]
Results imply that miR-487b decreases IL-6 and TNF-α expression, and both increased SOD and blocked MDA were identified in the CHF group. [score:3]
Compared with the CHF group, HW/BW and LVHW/BW were decreased in the miR-487b mimic and the si IL-33 groups (P < 0.05 for all), but increased in the miR-487b inhibitor group (P < 0.05 for both). [score:2]
Compared with the CHF group, there was an increase in SBP, DBP, LVSP, and ± dp/dt [max] but a decrease in LVEDP in the miR-487b mimic group and the si IL-33 group (P < 0.05 for all) and decline in SBP, DBP, LVSP, and ± dp/dt [max] in the miR-487b inhibitor group but an increase in LVEDP (P < 0.05 for all). [score:2]
Compared with the sham groups, rats in the miR-487b inhibitor group had differences, including increased heart volume, obvious inflammation, changed geometry, dark red heart, numerous pale infarcts, enlarged infarct size, increased ventricular aneurysm, and aggravated ventricle amplification (Figure 3). [score:2]
Compared with the CHF group, the miR-487b inhibitor group had an increase in MDA content but a decrease in SOD activity. [score:2]
Compared with the control group, the expressions of IL-6 and TNF-α were increased in the CHF group (P < 0.05 for both; Figure 1B), and that of miR-487b decreased in the CHF group (P < 0.05; Figure 1C). [score:2]
Inflammatory hypertrophy decreased and myocardial cells were disordered in the miR-487b inhibitor group, but the green collagen fibers were increased compared with the CHF group (Figure 4). [score:2]
LVPWs: left ventricular posterior wall thickness; LVPWd: left ventricular posterior wall thickness end-diastole; IVSs: systolic interventricular septum thickness; IVSd: interventricular septum thickness at end diastole; LVEF: left ventricular ejection fraction; CHF: chronic heart failure; miR-487b: microRNA-487b; NC: negative control. [score:1]
The 14q32 miRNA cluster belongs to one of the largest polycistronic clusters and consists of 54 miRNAs in humans and 61 in mice, and miR-487b is a member of this cluster [17]. [score:1]
CHF: chronic heart failure; HR: heart rate; SBP: systolic blood pressure; DBP: diastolic blood pressure; LVSP: left ventricular systolic pressure; LVEDP: left ventricular end diastolic pressure; miR-487b: microRNA-487b; NC: negative control. [score:1]
CHF: chronic heart failure; HW: heart weight; BW: body weight; LVW: left ventricular weight; miR-487b: microRNA-487b; NC: negative control. [score:1]
miR-487b: microRNA-487b; IL-33/ST2: interleukin-33/somatostatin 2; CHF: chronic heart failure. [score:1]
SOD: superoxide dismutase; MDA: malondialdehyde; CHF: chronic heart failure; miR-487b: microRNA-487b; NC: negative control; IL-33: interleukin-33. [score:1]
Figure 9 (A) Bioinformatics software for predicting the relation between miR-487b and IL-33; (B) a dual luciferase reporter system for verifying the relation between miR-487b and IL-33. [score:1]
The verification of the relation between miR-487b and IL-33. [score:1]
The number of apoptotic myocardial cells in each group were more than in the blank and sham groups (P < 0.05 for all), and the number in the si IL-33 and miR-487b mimic groups were less than that in the CHF group, but more than that in the blank and sham groups (P < 0.05 for all). [score:1]
CHF: chronic heart failure; miR-487b: microRNA-487b. [score:1]
org) was used to predict a correlation between miR-487b and IL-33 (Figure 9A). [score:1]
Figure 2CHF: chronic heart failure; miR-487b: microRNA-487b. [score:1]
CHF: chronic heart failure; IL-33: interleukin-33; ST2: somatostatin 2; TNF-a: tumor necrosis factor-α; miR-487b: microRNA-487b. [score:1]
In the si IL-33 and miR-487b mimic groups, the myocardial cells were dominant, and a few branching collagen fibers alternated with the myocardial cells. [score:1]
SOD activity and MDA in the si IL-33 group and the miR-487b mimic group were less than in the CHF group, but more than in the blank and sham groups. [score:1]
WT: wild type; MT: mutant; miR-487b: microRNA-487b; IL-33: interleukin-33. [score:1]
org) was used to predict the relation between miR-487b and IL-33, and a dual luciferase reporter system was used to verify the gene. [score:1]
A correlation was found between miR-487b and IL-33. [score:1]
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2
[+] score: 11
Other miRNAs from this paper: rno-mir-103-2, rno-mir-103-1, rno-mir-132, rno-mir-139, rno-mir-214
qRT-PCR analysis showed that the expression levels of miR-139-3p,-339-3p and -132-3p were up-regulated, and the expression levels of miR-487b, -2985 and -34b were down-regulated during bone loss (Fig. 2b). [score:11]
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3
[+] score: 6
According to the present study, several miRNAs were observed to target cholesterol metabolism -associated DEGs, including miR210, miR300-3p, miR-325-5p, miR-487b and miR-16. [score:3]
In addition, a number of miRNAs, including miR-16, miR-210, miR-15b, miR300-3p, miR-540, miR-325-5p and miR-487b, were observed to have target DEGs involved in cholesterol -associated metabolism, e. g. IDI1 and FDFT1. [score:3]
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4
[+] score: 3
Among these 21 differentially expressed miRNAs, 17 (miR-10b-5p, miR-223-3p, miR-208a-5p, miR-434-3p, miR-190a-5p, miR-30d-5p, miR-347, miR-493-5p, miR-29a-5p, miR-451-5p, miR-190b-5p, miR-466c-5p, miR-883-5p, miR-466b-1-3p, miR-21-3p, miR-3596c, miR3584-3p) were proven significant (P < 0.05) by qRT-PCR, one (miR-487b-3p) had a tendency to be significant (P = 0.06), and three (miR-138-2-3p, miR-1188-3p, miR-665) were not confirmed to be significant (Table  2). [score:3]
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5
[+] score: 2
analysis confirmed the direction and amplitude of all miRNA changes with the exception of let-7d, miR-25*, miR-187, miR-291a-5p, miR-292-5p, miR-365, miR-431, miR-487b, miR-615-5p, miR-743a, miR-20b-3p, miR-199a-3p which remained unaltered or showed no statistical significance. [score:2]
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6
[+] score: 1
9 -45.6 mmu-miR-27b -1.8 -71.4 -462.7 mmu-miR-214* -2.6 -5.0 -43.5 mmu-let-7c-1* -73.2 -204.4 -334.1 mmu-miR-34c -9.4 -26.1 -42.7 mmu-miR-542–3p -5.9 -195.6 -319.8 mmu-miR-706 -9.3 -5.0 -38.7 mmu-miR-487b -2.0 -161.5 -263.9 mmu-miR-467b* -10.1 -2.2 -33.6 rno-miR-17–3p -1.6 -152.0 -248.5 mmu-miR-323–3p -3.7 -23.3 -29.8 mmu-miR-10b -2. 4 -136.6 -223.3 mmu-miR-202–3p -6.5 -5.9 -21.4 mmu-miR-29b -3.0 -135.1 -220.9 mmu-miR-339–5p -1.6 -9.6 -19.6 mmu-miR-297a* -2.4 -128.4 -209.8 mmu-miR-181c -2.0 -10.5 -14.6 mmu-miR-692 -41.5 -115.8 -189.2 mmu-miR-203 -4.6 -6.4 -13.8 mmu-miR-208 -40.6 -113.5 -185.5 mmu-miR-467a* -2.6 -3.9 -11.4 mmu-miR-467c -38.9 -108.6 -177. [score:1]
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