Y‐box protein 1 promotes hypoxia/reoxygenation‐ or ischemia/reperfusion‐induced cardiomyocyte apoptosis via SHP‐1‐dependent STAT3 inactivation. Issue 11 (22nd January 2020)

• Record Type: Journal Article
• Authors: Cao, Xueming; Zhu, Na; Zhang, Yuwei; Chen, Yan; Zhang, Jing; Li, Jiang; Hao, Peiyuan; Gao, Chuanyu; Li, Li
• Is Part Of: Journal of cellular physiology. Volume 235:Issue 11(2020:Nov.)
• Page Start: 8187
• Page End: 8198
• Publication Date: 2020-01-22
• Subjects: acute myocardial infarction -- cardiomyocyte apoptosis -- hypoxia/reoxygenation -- ischemia/reperfusion -- SHP‐1 -- STAT3 -- Y‐box protein 1; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.29474
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: Cardiomyocyte apoptosis induced by hypoxia and ischemia plays important roles in heart dysfunction after acute myocardial infarction (AMI). However, the mechanism of apoptosis induction remains unclear. A previous study reported that Y‐box protein 1 (YB1) is upregulated after myocardial hypoxia/reoxygenation or ischemia/reperfusion (H/R or I/R, respectively) injury; however, whether YB1 is associated with H/R‐induced cardiomyocyte apoptosis is completely unknown. In the present study, we investigated the roles of YB1 in H/R‐induced cardiomyocyte apoptosis and the possible underlying molecular mechanisms. In vitro, H/R treatment upregulated the YB1 expression in H9C2 cells, whereas YB1 knockdown inhibited H/R‐induced cardiomyocyte apoptosis and induced H9C2 cell proliferation via Src homology region 2 domain‐containing phosphatase 1 (SHP‐1)‐mediated activation of signal transducer and activator of transcription 3 (STAT3). In vivo, YB1 knockdown ameliorated AMI, reducing infarct size, cardiomyocyte apoptosis, and oxidative stress, via SHP‐1‐mediated inactivation of STAT3. Additionally, YB1 knockdown inhibited H/R‐ or I/R‐induced oxidative stress in vitro and in vivo. H/R and I/R increase YB1 expression, and YB1 knockdown ameliorates AMI injury via SHP‐1‐dependent STAT3 inactivation. Abstract : 1. YB1 plays a critical role in AMI, and YB1 knockdown attenuates AMI injury via SHP‐1‐dependent STAT3 inactivation. 2. YB1 knockdown inhibited cardiomyocyte apoptosis. 3. YB1 knockdown decreases oxidative stress.