Knockdown of CkrL by shRNA deteriorates hypoxia/reoxygenation‐induced H9C2 cardiomyocyte apoptosis and survival inhibition Via Bax and downregulation of P‐Erk1/2. (20th February 2015)

• Record Type: Journal Article
• Authors: Zhang, Zhi‐Sheng; Yang, Dong‐Yan; Fu, Yan‐Bo; Zhang, Lei; Zhao, Qian‐Ping; Li, Gang
• Is Part Of: Cell biochemistry and function. Volume 33:Number 2(2015:Mar.)
• Page Start: 80
• Page End: 88
• Publication Date: 2015-02-20
• Subjects: Cytochemistry -- Periodicals; Cell metabolism -- Periodicals; Biochemistry -- Periodicals; Cytology -- Periodicals; 572
• DOI: 10.1002/cbf.3093
• Languages: English
• ISSNs: 0263-6484

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Integrin <italic>β</italic>1 subunit and its downstream molecule integrin‐linked kinase and focal adhesion kinase have been confirmed to be essential to cell survival and inhibition of apoptosis and hypoxia/reoxygenation (H/R)‐induced injuries in cardiomyocytes. However, it is still unclear whether CrkL [v‐crk avian sarcoma virus CT‐10 oncogene homolog (Crk)‐like], which acts also as a component of the integrin pathway, could also affect H/R‐induced injuries in the cardiomyocytes. The rat‐derived H9C2 cardiomyocytes were infected with a CrkL small hairpin RNA interference recombinant lentivirus, which knockdowns the endogenous CrkL expression in the cardiomyocytes. Apoptosis, cell proliferation and survival were examined in the H9C2 cardiomyocytes treated with either H/R or not. Results showed that knockdown of CrkL could significantly increase apoptosis and inhibition of the cell proliferation and survival and deteriorate the previously mentioned injuries induced by H/R. In contrast, overexpression of human CrkL could relieve the exacerbation of the previously mentioned injuries induced by CrkL knockdown in the H9C2 cardiomyocytes via regulation of Bax and extracellular signal‐regulated kinase1/2 (p‐ERK1/2). In conclusion, these results confirmed that knockdown of CrkL could deteriorate H/R‐induced apoptosis and cell survival inhibition in rat‐derived H9C2 cardiomyocytes via Bax and downregulation of p‐ERK1/2. It implies that CrkL could mitigate H/R‐induced injuries in the cardiomyocytes. Copyright © 2015 John Wiley & Sons, Ltd.</p> </abstract>