Downregulation of tripartite motif protein 11 attenuates cardiomyocyte apoptosis after ischemia/reperfusion injury via DUSP1‐JNK1/2. (10th November 2021)

• Record Type: Journal Article
• Authors: He, Fang; Wu, Zheqian; Wang, Yong; Yin, Lili; Lu, Shijie; Dai, Lihua
• Is Part Of: Cell biology international. Volume 46:Number 1(2022)
• Page Start: 148
• Page End: 157
• Publication Date: 2021-11-10
• Subjects: apoptosis -- caspase 3 -- ischemia/reperfusion injury -- JNK1/2 pathways -- TRIM11; Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.11716
• Languages: English
• ISSNs: 1065-6995

Abstract

Abstract: Currently, the prevention of ischemic diseases such as myocardial infarction associated with ischemia/reperfusion (I/R) injury remains to be a challenge. Thus, this study was designed to explore the effects of tripartite motif protein 11 (TRIM11) on cardiomyocytes I/R injury and its underlying mechanism. Cardiomyocytes AC16 were used to establish an I/R injury cell model. After TRIM11 downregulation in I/R cells, cell proliferation (0, 12, 24, and 48 h) and apoptosis at 48 h as well as the related molecular changes in oxidative stress‐related pathways was detected. Further, after the treatment of TRIM11 overexpression, SP600125, or DUSP1 overexpression, cell proliferation, apoptosis, and related genes were detected again. As per our findings, it was determined that TRIM11 was highly expressed in the cardiomyocytes AC16 after I/R injury. Downregulation of TRIM11 was determined to have significantly reduced I/R‐induced proliferation suppression and apoptosis. Besides, I/R‐activated c‐Jun N‐terminal kinase (JNK) signaling and cleaved caspase 3 and Bax expression were significantly inhibited by TRIM11 downregulation. In addition, the overexpression of TRIM11 significantly promoted apoptosis in AC16 cells, and JNK1/2 inhibition and DUSP1 overexpression potently counteracted the induction of TRIM11 overexpression in AC16 cells. These suggested that the downregulation of TRIM11 attenuates apoptosis in AC16 cells after I/R injury probably through the DUSP1‐JNK1/2 pathways.