IL-20 promotes hypoxia/reoxygenation-induced mitochondrial dysfunction and apoptosis in cardiomyocytes by upregulating oxidative stress by activating the PKC/NADPH oxidase pathway

Kun Ling Tsai, Pei Ling Hsieh, Wan Ching Chou, Ching Hsia Hung, Hsin Lun Yang, Yun Ching Chang, Pei Ming Chu, Ming Shi Chang, Shih Hung Chan

研究成果: Article

摘要

Acute myocardial infarction (AMI) is the maximum critical cardiovascular event and causes high morbidity and mortality worldwide. The ischemia and reperfusion that occur in AMI cause apoptosis and cellular dysfunction in cardiomyocytes. IL-20, an IL-10 family member, is involved in various inflammatory diseases. Therefore, we sought to elucidate the role of IL-20 in the infarcted heart following ischemia/reperfusion (I/R) injury. We found that IL-20 and its receptors, IL-20R1 and IL-20R2, were increased in H2C2 cardiomyoblast cells and ventricular tissues subjected to hypoxia/reoxygenation (H/R) stimulation. The presence of IL-20 further inhibited the cell viability of H9C2 cells and primary cardiomyocytes. Our results suggested that IL-20 elicited an increase in Ca2+ and activation of the PKC/NADPH oxidase pathway, leading to the elevation of oxidase stress and downregulation of AKT. Furthermore, we demonstrated that IL-20 was able to mediate H/R-induced apoptosis via PKC/NADPH oxidase/AKT signaling. Our findings implied that IL-20 was responsive to H/R stress in vitro and in rat hearts undergoing I/R injury, and this upregulation of IL-20 may contribute to the apoptosis of cardiomyocytes.

原文English
文章編號165684
期刊Biochimica et Biophysica Acta - Molecular Basis of Disease
1866
發行號5
DOIs
出版狀態Published - 2020 五月 1

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All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Molecular Biology

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