MicroRNA-93 inhibits ischemia-reperfusion induced cardiomyocyte apoptosis by targeting PTEN

Ke, Zun‐Ping; Xu, Peng; Shi, Yan; Gao, Ai-Mei

doi:10.18632/oncotarget.8941

Cited by 89 publications

(72 citation statements)

References 17 publications

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“…In previous years, an increasing number of studies focusing on the upstream regulatory factors of PTEN have revealed that certain lncRNAs and miRNAs may regulate their expression in a variety of ways. Ke et al (45) indicated that miR-93 may protect against HR-induced cardiomyocyte apoptosis by inhibiting the PI3K/AKT/PTEN signaling pathway. It has also been reported that lncRNAs may directly or indirectly regulate PTEN during apoptosis in tumor cells (46).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA GAS5 regulates myocardial ischemia‑reperfusion injury through the PI3K/AKT apoptosis pathway by sponging miR‑532‑5p

Han

Xia

et al. 2020

Int J Mol Med

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Long non-coding RNAs (lncRNAs) have been revealed to have a marked effect in cardiovascular diseases, including during cardiac development, cardiac hypertrophy, myocardial fibrosis and myocardial ischemic injury. The mechanism of myocardial ischemia-reperfusion injury (MIRI) is very complicated. Although studies have confirmed that lncRNAs are involved, the specific mechanism remains largely unknown. The lncRNA growth arrest specific 5 (GAS5) is known as a regulator of a number of diseases, including certain cancer types. The present study aimed to investigate the function of lncRNA GAS5 in MIRI. The present study reported that the expression of lncRNA GAS5 in H9c2 cells treated with anoxia and reoxygenation was significantly upregulated compared with the control group (P<0.05). Similarly, the expression of lncRNA GAS5 in myocardial tissue obtained from rats treated with MIRI was significantly upregulated compared with the untreated controls (P<0.05). Silencing of lncRNA GAS5 was able to attenuate myocardial damage, as cell viability increased and the apoptosis rate decreased. classical apoptotic proteins involved in MIRI, including B-cell lymphoma 2, Bcl-2-associated X protein and cleaved caspase-3, also exhibited the same trend. At the same time, when lncRNA GAS5 was silenced, microRNA (miR)-532-5p, which was originally expressed at the stage of injury, was upregulated. The luciferase reporter assay results indicated that the lncRNA GAS5 functioned as a molecular sponge of miR-532-5p. The gain-and loss-of-function analysis of miR-532-5p indicated that it was involved in the regulation of MIRI; the trend of results following its overexpression was also consistent with the trend observed following the silencing of lncRNA GAS5. Notably, the protective effect of lncRNA GAS5 silencing on cells was attenuated by miR-532-5p inhibition. Phosphatase and tensin homolog was revealed to be a key target gene for the function of lncRNA GAS5, and its regulation was achieved via binding to miR-532-5p. In other words, silencing lncRNA GAS5 ultimately promoted the activation of the phosphoinositide-3-kinase (PI3K)/protein kinase B pathway (AKT) to reduce myocardial damage. Therefore, lncRNA GAS5 was able to regulate MIRI through the PI3K/AKT apoptosis pathway by sponging miR-532-5p.

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Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA GAS5 regulates myocardial ischemia‑reperfusion injury through the PI3K/AKT apoptosis pathway by sponging miR‑532‑5p

Han

Xia

et al. 2020

Int J Mol Med

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“…Subsequently, by detecting the activities of serum myocardial enzymes that are regarded as markers of ischemic myocardial damage, we found that the expression level of miR-24-3p in ischemia/reperfusion mice was negatively correlated with the levels of serum lactate dehydrogenase, creatine kinase and creatine kinase-mb form (LDH, CK and CK-MB) [18,19]. Patients with ischemic heart disease usually suffer from myocardial reperfusion after therapy, which might result in acute myocardial damage and adverse ventricular remodeling [20,21].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-24-3p Attenuates Myocardial Ischemia/Reperfusion Injury by Suppressing RIPK1 Expression in Mice

Tan¹,

Qi²,

Fan³

et al. 2018

Cell Physiol Biochem

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Background/Aims: This study was developed to investigate a potential therapeutic method for myocardial ischemia/reperfusion injury involving the promotion of miR-24-3p expression. Methods: Microarray analysis was used to screen differentially expressed genes in a myocardial ischemia/reperfusion (I/R) injury mouse model. Gene set enrichment analysis was utilized to determine vital signaling pathways. Targeting verification was conducted with a luciferase reporter assay. Myocardial I/R injury was developed in mice, and the expression levels of RIPK1 and miR-24-3p were investigated by qRT-PCR and Western blot. Hemodynamic parameters and the activity of serum myocardial enzymes were measured to evaluate cardiac function. Infarct area was observed through HE and TTC staining. Myocardial cell apoptosis was examined by TUNEL staining and caspase-3 activity analysis. Results: RIPK1 was an upregulated mRNA found by microarray analysis and a verified target of the downregulated miRNA miR-24-3p. The upregulation of RIPK1 (1.8-fold) and the downregulation of miR-24-3p (0.3-fold) were confirmed in I/R mice. RIPK1 led to impaired cardiac function indexes, increased infarct area and cell apoptosis, while miR-24-3p could reverse the injury by regulating RIPK1. The TNF signaling pathway was proven to be involved in myocardial I/R injury through the detection of the dysregulation of related proteins. Conclusion: In conclusion, RIPK1 was upregulated and miR-24-3p was downregulated in a myocardial I/R injury mouse model. RIPK1 could aggravate myocardial I/R injury via the TNF signaling pathway, while miR-24-3p could suppress RIPK1 and therefore exert cardioprotective effects in myocardial I/R injury.

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“…Consistent with the reduced S‐sulfhydration, Akt activity increased significantly (Ohno et al, ). As far as we know, PTEN is also a key signal molecular in cardiomyocyte apoptosis (Ke et al, ), ventricular remodelling (Yang et al, ), angiogenesis (Serra et al, ) and other cardiovascular diseases. It is thought that protein S‐sulfhydration and S‐nitrosylation of PTEN keep a dynamic balance, and compete with each other to maintain normal function of the protein.…”

Section: Crosstalk With Protein S‐sulfhydration and Other Post‐translmentioning

confidence: 99%

Protein S‐sulfhydration by hydrogen sulfide in cardiovascular system

Meng

Zhao

Xie

et al. 2017

British J Pharmacology

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MicroRNA-93 inhibits ischemia-reperfusion induced cardiomyocyte apoptosis by targeting PTEN

Cited by 89 publications

References 17 publications

Long non‑coding RNA GAS5 regulates myocardial ischemia‑reperfusion injury through the PI3K/AKT apoptosis pathway by sponging miR‑532‑5p

Long non‑coding RNA GAS5 regulates myocardial ischemia‑reperfusion injury through the PI3K/AKT apoptosis pathway by sponging miR‑532‑5p

MicroRNA-24-3p Attenuates Myocardial Ischemia/Reperfusion Injury by Suppressing RIPK1 Expression in Mice

Protein S‐sulfhydration by hydrogen sulfide in cardiovascular system

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