miR-9 knockdown inhibits hypoxia-induced cardiomyocyte apoptosis by targeting Yap1

Zheng, Jiayong; Peng, Bangtian; Zhang, Yanwei; Ai, Feng; Hu, Xiaosong

doi:10.1016/j.lfs.2019.01.014

Cited by 26 publications

(15 citation statements)

References 28 publications

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“…Although its effect on cardiomyocyte apoptosis has not been studied in detail in the past, many studies have been conducted on the effect of miRNA on cardiomyocyte apoptosis. For example, some studies [22] have reported that miR-9 can inhibit hypoxia-induced cardiomyocyte apoptosis by targeting Yap1. Another study [23] has pointed out that miR-486 can regulate apoptosis of cardiomyocytes by regulating Bcl-2.…”

Section: Discussionmentioning

confidence: 99%

Effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure by regulating TGF-β1/Smad3 signaling pathway

Xie

Lei

et al. 2020

Bioscience Reports

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Purpose: The present study set out to investigate the effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure (HF) and its mechanism. Methods: HF rat model and hypoxia/reoxygenation (H/R) cardiomyocyte model were established. miR-195-5p expression and transforming growth factor-β1 (TGF-β1)/signal transduction protein (Smad)3 signaling pathway in HF rats and H/R cardiomyocytes were interfered. miR-195-5p expression was tested by Rt-PCR, TGF-β1/Smad3 signaling pathway related proteins were detected by Western Blot, apoptosis of HF rat cardiomyocytes was tested by TUNEL, and apoptosis of cardiomyocytes induced by H/R was checked by flow cytometry. Results: miR-195-5p was lowly expressed in myocardium of HF rats, while TGF-β1 and Smad3 proteins were high-expressed. Up-regulating miR-195-5p expression could obviously inhibit cardiomyocyte apoptosis of HF rats, improve their cardiac function, and inhibit activation of TGF-β1/Smad3 signaling pathway. Up-regulation of miR-195-5p expression or inhibition of TGF-β1/Smad3 signaling pathway could obviously inhibit H/R-induced cardiomyocyte apoptosis. Dual-luciferase reporter enzyme verified the targeted relationship between miR-195-5p and Smad3. Conclusion: miR-195-5p can inhibit cardiomyocyte apoptosis and improve cardiac function in HF rats by regulating TGF-β1/Smad3 signaling pathway, which may be a potential target for HF therapy.

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Section: Discussionmentioning

confidence: 99%

Effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure by regulating TGF-β1/Smad3 signaling pathway

Xie

Lei

et al. 2020

Bioscience Reports

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“…Previous studies have shown that the down-regulation of miR-532-5p in myocardium H9c2 cells and in myocardial infarction-affected rats under hypoxia stress can up-regulate the expression of its target gene encoding programmed cell death protein 4, and promote the expression of CASPASE-3, thereby increasing H9c2 apoptosis (Ma et al, 2018). In addition, inhibition of miR-9 can up-regulate the expression of the gene encoding Yesassociated protein 1, promote cell proliferation, and inhibit CASPASE-3/7 activity and apoptosis in hypoxic H9c2 cells (Zheng et al, 2019).…”

Section: Regulation Mechanisms Of Gift Injected With Mirna Antagomir mentioning

confidence: 99%

miR-34a Regulates the Activity of HIF-1a and P53 Signaling Pathways by Promoting GLUT1 in Genetically Improved Farmed Tilapia (GIFT, Oreochromis niloticus) Under Hypoxia Stress

et al. 2020

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In fish under hypoxia stress, homeostasis can become imbalanced, leading to tissue and organ damage and decreased survival. Therefore, it is useful to explore the molecular and physiological regulation mechanisms that function in fish under hypoxia stress. The microRNA miR-34a is involved in fat and glycogen metabolism, and in apoptosis. In this study, we first verified that GLUT1, the gene encoding glucose transporter 1, is a potential target gene of miR-34a in genetically improved farmed tilapia (GIFT, Oreochromis niloticus) by dual luciferase reporter assays. Then, we clarified the regulatory relationship between miR-34a and GLUT1 by qRT-PCR analyses. We analyzed the regulatory effects of knockdown or promotion of GLUT1 expression in vitro and in vivo in GIFT under hypoxia stress. The results confirm that GLUT1 is a target gene of miR-34a in GIFT. Down-regulation of miR-34a significantly promoted GLUT1 expression. Knockdown of GLUT1 reduced the glycogen content in GIFT liver cells, inhibited HIF-1a gene expression, up-regulated the expression of genes involved in P53 signaling pathways (P53 and CASPASE-3 genes), and accelerated hepatocyte apoptosis under hypoxia stress. Compared with the control group, the group injected in the tail vein with miR-34a antagomir showed up-regulated expression of GLUT1 in the liver, increased liver glycogen content at 96 h of hypoxia stress, down-regulated expression of P53 and CASPASE-3, and decreased serum aspartate aminotransferase and alanine aminotransferase enzyme activities. Our results provide information about the molecular regulation mechanism of miRNAs and their target genes in fish during the response to hypoxia stress.

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“…In another study, downregulation of miR-532-5p expression in H9c2 cells exposed to hypoxia led to up-regulation of its target gene encoding programmed cell death protein 4, and increased the expression of caspase-3, thereby promoting hypoxia-induced apoptosis of H9c2 cells (Ma et al, 2018). Inhibition of miR-9 up-regulated the gene encoding Yes-associated protein 1, promoted cell proliferation, and inhibited apoptosis and caspase-3/7 activity in hypoxic H9c2 cells (Zheng et al, 2019).…”

Section: Discussionmentioning

confidence: 93%

Hypoxia-induced miR-92a regulates p53 signalling pathway and apoptosis by targeting calcium-sensing receptor in Genetically Improved Farmed Tilapia (Oreochromis niloticus)

Qiang

Tao

Bao

et al. 2020

Preprint

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AbstractmiR-92a miRNAs are immune molecules that regulate apoptosis (programmed cell death) during the immune response. Apoptosis helps to maintain the dynamic balance in tissues of fish under hypoxia stress. The aim of this study was to explore the role and potential mechanisms of miR-92a in the liver of tilapia under hypoxia stress. We first confirmed that CaSR (encoding a calcium-sensing receptor) is a target gene of miR-92a in genetically improved farmed tilapia (GIFT) using luciferase reporter gene assays. In GIFT under hypoxia stress, miR-92a was up-regulated and CaSR was down-regulated in a time-dependent manner. Knocked-down CaSR expression led to inhibited expression of p53, TP53INP1 and caspase-3/8, reduced the proportion of apoptotic hepatocytes, and decreased the activity of calcium ions induced by hypoxia in hepatocytes. GIFT injected in the tail vein with an miR-92a agomir showed up-regulation of miR-92a and down-regulation of CaSR, p53, TP53INP1, and caspase-3/8 genes in the liver, resulting in lower serum alanine aminotransferase and aspartate aminotransferase activities under hypoxia stress. These findings suggest that stimulation of miR-92a interferes with hypoxia-induced apoptosis in hepatocytes of GIFT by targeting CaSR, thereby alleviating liver damage. These results provide new insights into the adaptation mechanisms of GIFT to hypoxia stress.

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miR-9 knockdown inhibits hypoxia-induced cardiomyocyte apoptosis by targeting Yap1

Cited by 26 publications

References 28 publications

Effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure by regulating TGF-β1/Smad3 signaling pathway

Effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure by regulating TGF-β1/Smad3 signaling pathway

miR-34a Regulates the Activity of HIF-1a and P53 Signaling Pathways by Promoting GLUT1 in Genetically Improved Farmed Tilapia (GIFT, Oreochromis niloticus) Under Hypoxia Stress

Hypoxia-induced miR-92a regulates p53 signalling pathway and apoptosis by targeting calcium-sensing receptor in Genetically Improved Farmed Tilapia (Oreochromis niloticus)

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