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12 publications mentioning rno-mir-675

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-675. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 76
However, enforced expression of miR-675 could suppress apoptosis in cardiomyocytes with H19 siRNA transfection, suggesting that H19 downregulation promotes apoptosis via inhibition of miR675 (Fig. 4C,D). [score:10]
However, knockdown of VDAC1 could inhibit apoptosis in cardiomyocytes with miR-675 antagomir transfection, suggesting that miR-675 downregulation induces apoptosis by increasing VDAC1 expression (Fig. 5C–E). [score:9]
The expression of miR-675 was downregulated in cardiomyocytes transfected with H19 siRNA, which consequently resulted in increased apoptosis. [score:6]
The expression of VDAC1 was upregulated in cardiomyocytes transfected with miR-675 antagomir, which consequently contributed to increased apoptosis. [score:6]
In the present study, our findings demonstrated that the H19/miR-675 axis participated in the regulation of mitochondrial apoptotic pathway by targeting VDAC1. [score:4]
In this study, we found that both miR-675 and its precursor H19 were downregulated in cardiomyocytes exposed to high glucose. [score:4]
To confirm whether VDAC1 was a direct target of miR-675, we performed luciferase reporter experiments in HEK293 cells. [score:4]
How to cite this article: Li, X. et al. lncRNA H19/miR-675 axis regulates cardiomyocyte apoptosis by targeting VDAC1 in diabetic cardiomyopathy. [score:4]
Apoptosis-related gene VDAC1 is a direct target of miR-675. [score:4]
Among the putative targets of miR-675, we focused on VDAC1, which belongs to the mitochondrial porin family and is involved in the modulation of apoptosis (Fig. 5A). [score:3]
Among the putative targets of miR-675, we focused on VDAC1, a gene encoding a voltage -dependent anion channel protein as a major component of the outer mitochondrial membrane. [score:3]
The luciferase assay indicated that VDAC1 was a direct target of miR-675 (Fig. 5B). [score:3]
The miR-675 expression was determined by real-time PCR. [score:3]
In summary, these data revealed a novel function of H19/miR-675/VDAC1 pathway in the regulation of high glucose -mediated apoptosis, which may provide valuable insights for understanding the pathogenic role of lncRNA H19 in the development of DCM. [score:3]
The results of luciferase assay suggested that VDAC1 might be a direct target of miR-675. [score:3]
We then performed in vitro experiments using cultured neonatal rat cardiomyocytes, and our findings revealed that high glucose could induce apoptosis by regulating H19/miR-675/VDAC1 pathway. [score:2]
H19/miR-675 axis is involved in the regulation of high glucose -induced apoptosis. [score:2]
We cloned the 3′UTR of VDAC1 downstream of a luciferase reporter construct and cotransfected it into HEK293 cells with miR-675 mimic. [score:1]
The 3′-UTR of VDAC1 was fused to the luciferase coding region and transfected into HEK293 cells with miR-675 mimic. [score:1]
The 3′-UTR without predicted miR-675 binding site was constructed to generate Luc-VDAC1-Mut vector. [score:1]
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2
[+] score: 68
The expression of H19 and miR-675 was significantly upregulated in the myocardium of DCM rats and downregulated after administration of lentivirus H19-shRNA (Figure 1A). [score:9]
H19 was found to induce myocardial apoptosis by upregulating miR675, which consequently inhibited the expression of anti-apoptosis gene PA2G4. [score:8]
The expression of miR-675 was upregulated in cardiomyocytes treated with adriamycin. [score:6]
In addition, H19 can also function as a precursor of miR-675 to post-translationally modulate several target genes involved in various cell processes [7– 9]. [score:5]
In this study, our findings indicated that H19 was upregulated in the myocardium of DCM rats and H19/miR-675 axis was associated with cardiomyocyte apoptosis. [score:4]
To determine whether PA2G4 was a direct target of miR-675, we performed luciferase reporter experiments in HEK293 cells. [score:4]
In the present study, our findings suggested that H19/miR-675 axis could participate in the regulation of adriamycin -induced cardiomyocyte apoptosis by targeting EBP1. [score:4]
In this study, we found that both miR-675 and its precursor H19 were upregulated in cardiomyocytes exposed to adriamycin. [score:4]
Our results showed that PA2G4 was a direct target of miR-675 (Figure 4A, 4B). [score:4]
Enforced expression of miR-675 could increase apoptosis in cardiomyocytes with adriamycin treatment and H19-siRNA transfection (Figure 3C, 3D). [score:3]
Figure 1 (A) The expression of H19 and miR-675 in myocardium was detected by real-time PCR. [score:3]
Figure 4 (A) PA2G4 was predicted as a target gene of miR-675 using miRBase. [score:3]
Moreover, the results of luciferase reporter assay suggested that PA2G4 might be a direct target of miR-675. [score:3]
The expression of PA2G4 was reduced in cardiomyocytes transfected with miR-675 mimic and increased after transfected with miR-675 antagomir (Figure 4C, 4D). [score:3]
In conclusion, our study revealed a novel function of H19/miR-675/PA2G4 pathway in the regulation of cardiomyocyte apoptosis, which will provide valuable insights into understanding the pathological mechanisms of adriamycin -induced DCM. [score:2]
To determine whether PA2G4 is the target gene of miR-675, we conducted luciferase reporter assay in HEK293 cells. [score:2]
The 3′-UTR without predicted miR-675 binding site was constructed to generate Luc-PA2G4-Mut vector. [score:1]
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3
[+] 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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4
[+] score: 24
There are two regulatory types of H19: on one hand, it can encode miR-675 from its first exon, inhibiting its target genes 17, 39; on the other hand, it can function as a ceRNA to bind a series of miRNAs including let-7b 18, 22, 23, derepressing their targets. [score:8]
Zhuang M Gao W Xu J Wang P Shu Y The long non-coding RNA H19-derived miR-675 modulates human gastric cancer cell proliferation by targeting tumor suppressor RUNX1Biochem. [score:5]
Ma L Long noncoding RNA H19 derived miR-675 regulates cell proliferation by down -regulating E2F-1 in human pancreatic ductal adenocarcinomaJ. [score:3]
Steck E Regulation of H19 and its encoded microRNA-675 in osteoarthritis and under anabolic and catabolic in vitro conditionsJ. [score:2]
Wang J Wang X Chen T Jiang L Yang Q Huaier extract inhibits breast cancer progression through a LncRNA-H19/MiR-675-5p pathwayCell. [score:2]
The previous studies reveal that H19 enhances tumorigenesis, metastasis, and invasion of different kinds of tumor cells through encoding miRNA-675, such as pancreatic ductal adenocarcinoma [40], breast cancer 41, 42, gastric cancer [43], and glioma [19]. [score:1]
Dey BK Pfeifer K Dutta A The H19 long noncoding RNA gives rise to microRNAs miR-675-3p and miR-675-5p to promote skeletal muscle differentiation and regenerationGenes Dev. [score:1]
In this study, miR-675 (both miR-675-3p and miR-675-5p) levels in the hippocampus of the rat after SE was not changed (data not shown). [score:1]
However, the present results with no changes of miR-675 after SE suggest that H19 might not act by encoding miR-675 during epileptogenesis in TLE. [score:1]
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5
[+] score: 10
miR-483 and miR-675 appear to be a pair of intragenic miRNAs that regulate the expression of this imprinting region. [score:4]
However, the dysexpression of miR-483 in liver fibrosis and HCC might result from other mechanism, such as H19 gene and its intragenic miRNA miR-675. [score:3]
The long non-coding RNA H19 functions as a precursor of miR-675, which in turn suppresses Igf1r [30, 31]. [score:3]
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6
[+] score: 9
Other miRNAs from this paper: rno-mir-22, rno-mir-141
In addition, miR-675-5p directly targets H19, and H19 enhances osteogenesis through activating the Wnt/β-catenin signaling pathway [11]. [score:4]
Furthermore, overexpression of lncRNA H19 promotes the proliferation of T/G HA-VSMC in miR-675 in vitro [30]. [score:3]
MiRNAs, such as miR-675, also regulate lncRNAs in glioma [29]. [score:2]
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7
[+] score: 7
Our previous work also revealed that the heart failure of the rat with selenium deficiency was probably related to five upregulated miRNAs (miR-374, miR-16, miR-199a-5p, miR-195 and miR-30e) and three downregulated miRNAs (miR-3571, miR-675 and miR-450a) [11]. [score:7]
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8
[+] score: 5
Furthermore, male expression was higher than female expression for all except one (miR-675*) of the two-week-specific miRNAs. [score:5]
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9
[+] score: 4
Several miRNAs are demonstrated that associated with OA development and modulation such as miR-18a (chondrocyte differentiation), miR-27b (controlling the expression of MMP-13), miR-34a (prevention of cartilage degradation), miR-140 and miR-222 (controlling cartilage homeostasis), miR-146 (promotion of inflammatory OA), miR146a (OA cartilage pathogenesis), miR-675 (cartilage repair) [30, 31]. [score:4]
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10
[+] score: 3
Other miRNAs from this paper: rno-mir-22
[2] Recently, Li et al. [14] demonstrated that H19/miR-675 axis was involved in the modulation of hyperglycemia -induced apoptosis by targeting VDAC1, which may provide a novel therapeutic strategy for DCM. [score:3]
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11
[+] score: 2
Furthermore, H19 can serve as a precursor of miR-675 and regulate carcinogenesis, progression and metastasis of several types of cancers [10– 12]. [score:2]
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12
[+] score: 1
Dey BK Pfeifer K Dutta A The h19 long noncoding rna gives rise to micrornas mir-675-3p and mir-675-5p to promote skeletal muscle differentiation and regenerationGenes Dev. [score:1]
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