WDR26 promotes mitophagy of cardiomyocytes induced by hypoxia through Parkin translocation

Feng, Yan; Zhao, Jia; Hou, Huifang; Zhang, Hui; Jiao, Yunjuan; Wang, Jiangang; Wang, Yongling; Sun, Yan

doi:10.1093/abbs/gmw104

Cited by 27 publications

(20 citation statements)

References 44 publications

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“…Patients with AMI always present severe and persistent pain in the chest, which can be combined with arrhythmia, shock, or heart failure [ 4 , 5 ]. Oxidative stress plays an important role in cardiomyocyte proliferation and differentiation [ 6 ]. Hypoxia disrupts microenvironment homeostasis, leading to cardiomyocyte cell apoptosis [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

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Knockdown of MicroRNA-122 Protects H9c2 Cardiomyocytes from Hypoxia-Induced Apoptosis and Promotes Autophagy

Zhang¹,

Li²,

Chen³

et al. 2017

Med Sci Monit

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BackgroundAcute myocardial infarction (AMI) is a severe disease causing heart failure and sudden death. Studies indicate that microRNAs (miRNAs) are involved in the pathophysiology of AMI. In the present study, we carefully explored the effects of miR-122 on myocardial hypoxia injury and its possible underlying mechanism.Material/MethodsmiR-122 expression was analyzed in H9c2 cardiomyocytes after being transfected with miR-122 mimic, ASO-miR-122, or negative control. Cell viability and apoptosis were investigated by CCK-8 assays and flow cytometry analysis, respectively. Cell migration was analyzed using wound-healing assays. Western blotting was performed to analyze the expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN)/phosphatidylinositol 3-hydroxy kinase (PI3K)/AKT and LC3-II/LC3-I.ResultHypoxia exposure significantly inhibited H9c2 cell viability (P<0.01). miR-122 overexpression promoted the hypoxia-induced H9c2 cell proliferation and migration loss (P<0.05), and cell apoptosis was increased (P<0.05). miR-122 knockdown enhanced cell viability and decreased cell apoptosis (P<0.05). Knockdown of miR-122 enhanced PTEN/PI3K/AKT activation and cell autophagy. Overexpression of miR-122 inhibited the PTEN/PI3K/AKT pathway and cell autophagy pathway.ConclusionsThe expression of miR-122 is involved in hypoxia-induced H9c2 cardiomyocyte injury. Knockdown of miR-122 protects H9c2 cells from hypoxia-induced apoptosis and enhances cell viability.

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Section: Introductionmentioning

confidence: 99%

“…Oxidative stress plays an important role in cardiomyocyte proliferation and differentiation [ 6 ]. Hypoxia disrupts microenvironment homeostasis, leading to cardiomyocyte cell apoptosis [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of MicroRNA-122 Protects H9c2 Cardiomyocytes from Hypoxia-Induced Apoptosis and Promotes Autophagy

Zhang¹,

Li²,

Chen³

et al. 2017

Med Sci Monit

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show abstract

“…However, the injury of ischemic myocardial tissue will be aggravated in case that blood supply in myocardium is recovered, therefore causing myocardial ischemia reperfusion injury (Hernandez-Resendiz et al 2018 ). Myocardial cell injury could be caused by cell necrosis and apoptosis (Feng et al 2016 ). Hypoxia can damage the microenvironment homeostasis, leading to myocardial cell apoptosis and aggravating the condition of AMI (Zhang et al 2017 ).…”

Section: Introductionmentioning

confidence: 99%

MiR-499 inhibited hypoxia/reoxygenation induced cardiomyocytes injury by targeting SOX6

Shi

Yun-feng²,

Niu³

et al. 2019

Biotechnol Lett

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Objective MiR-499 has been reported to be expressed only in cardiomyocytes, and its expression would increase after acute myocardial infarction (AMI). miR-499 plays a role in the process of cardiomyocytes injury induced by hypoxia/reoxygenation (H/R), however, it still remains unclear. Results Hypoxia inhibited miR-499-5p expression and H/R induced apoptosis. SOX6 was a target gene of miR-499-5p, and high expression of miR-499-5p inhibited the expression of SOX6. MiR-499-5p reduced H9c2 cells injury by inhibiting the expression of SOX6, overexpression of which could reverse the effect of miR-499-5p on H9c2 cells. MiR-499-5p inhibited the levels of LDH and MDA, while overexpression of miR-499-5p inhibited H/R-induced cell apoptosis. MiR-499-5p could up-regulate the level of Bcl-2 and down-regulate the expression levels of Bax and caspase-3. However, SOX6 partially reversed these effects of miR-499-5p. Conclusion We proved that miR-499-5p inhibited H/R-induced cardiomyocytes injury by targeting SOX6. Our results suggested that miR-499-5p/SOX6 pathway may present a potential therapeutic target for the treatment of AMI.

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“…Myocardial infarction is defined as necrosis of cardiomyocytes as a result of prolonged ischaemia, which is responsible for heart failure, cardiac fibrosis and sudden death . Oxidative stress plays an important role in cardiomyocyte proliferation, apoptosis and differentiation . Currently, stem cell therapies for myocardial infarction have become promising alternatives to repair and regenerate injured tissues, and their applications are being extensively studied in various diseases …”

Section: Introductionmentioning

confidence: 99%

Induced pluripotent stem cell‐conditional medium inhibits H9C2 cardiomyocytes apoptosis via autophagy flux and Wnt/β‐catenin pathway

Guo

Sohun

et al. 2019

J Cellular Molecular Medi

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Induced pluripotent stem cell‐derived conditioned medium ( iPS ‐ CM ) could improve cell viability in many types of cells and may be a better alternative for the treatment of myocardial infarction. This study aimed to examine the influence of iPS ‐ CM on anti‐apoptosis and the proliferation of H9C2 cardiomyocytes and investigate the underlying mechanisms. H9C2 cardiomyocytes were exposed to 200 μmol/L hydrogen peroxide (H 2 O 2 ) for 24 hours with or without pre‐treatment with iPS ‐ CM . The ratio of apoptotic cells, the loss of mitochondrial membrane potential (△Ψm) and the levels of intracellular reactive oxygen species were analysed by flow cytometric analysis. The expression levels of BCL ‐2 and BAX proteins were analysed by Western blot. Cell proliferation was assessed using cell cycle and EdU staining assays. To study cell senescence, senescence‐associated β‐galactosidase ( SA ‐β‐gal) staining was conducted. The levels of malondialdehyde, superoxide dismutase and glutathione were also quantified using commercially available enzymatic kits. The results showed that iPS ‐ CM containing basic fibroblast growth factor significantly reduced H 2 O 2 ‐induced H9C2 cardiomyocyte apoptosis by activating the autophagy flux pathway, promoted cardiomyocyte proliferation by up‐regulating the Wnt/β‐catenin pathway and inhibited oxidative stress and cell senescence. In conclusion, iPS ‐ CM effectively enhanced the cell viability of H9C2 cardiomyocytes and could potentially be used to inhibit cardiomyocytes apoptosis to treat myocardial infarction in the future.

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WDR26 promotes mitophagy of cardiomyocytes induced by hypoxia through Parkin translocation

Cited by 27 publications

References 44 publications

Knockdown of MicroRNA-122 Protects H9c2 Cardiomyocytes from Hypoxia-Induced Apoptosis and Promotes Autophagy

Knockdown of MicroRNA-122 Protects H9c2 Cardiomyocytes from Hypoxia-Induced Apoptosis and Promotes Autophagy

MiR-499 inhibited hypoxia/reoxygenation induced cardiomyocytes injury by targeting SOX6

Induced pluripotent stem cell‐conditional medium inhibits H9C2 cardiomyocytes apoptosis via autophagy flux and Wnt/β‐catenin pathway

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