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Tissue transglutaminase 2 promotes apoptosis of rat neonatal cardiomyocytes under oxidative stress

Title
Tissue transglutaminase 2 promotes apoptosis of rat neonatal cardiomyocytes under oxidative stress
Authors
Heesang Song;Byoung-Keuk Kim;Ki-Chul Hwang;Yangsoo Jang;Min-Ji Cha;Byeong-Wook Song;Soyeon Lim;Woochul Chang
Issue Date
2011
Journal Title
Journal of Receptors and Signal Transduction Research
ISSN
1079-9893
Citation
Journal of Receptors and Signal Transduction Research, Vol.31(1) : 66~74, 2011
Abstract
The role of tissue transglutaminase 2 (TG2) in cardiac myocyte apoptosis under oxidative stress induced by ischemic injury remains unclear. Here, we investigated the effects of TG2 on apoptosis of cardiomyocytes under oxidative stress. Ectopic expression of TG2 increased caspase-3 activity and calcium overload in cardiomyocytes. Expression levels of TG2 were significantly increased in H(2)O(2)-treated cardiomyocytes. Caspase-3 activity assay demonstrated its considerable correlation with TG2 expression, which supported that caspase-3 inhibitor inhibited the apoptosis induced by the ectopic overexpression of TG2. In addition, the other apoptotic signals, such as caspase-8, cytochrome c, and Bax, were increased dependent with TG2 expression in H(2)O(2)-treated cardiomyocytes. These results indicated that apoptotic signals had a positive correlation with TG2 expression. The decreased expression of phospholipase C (PLC)-δ1 and phospho-PKC in H(2)O(2)-treated cardiomyocytes were rescued by TG2 silencing. Together, our data strongly suggest that oxidative stress up-regulates TG2 expression in cardiomyocytes, leading to apoptosis.
URI
http://informahealthcare.com/doi/abs/10.3109/10799893.2010.529577

http://ir.ymlib.yonsei.ac.kr/handle/22282913/92585
DOI
10.3109/10799893.2010.529577
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Internal Medicine
1. 연구논문 > 1. College of Medicine > Yonsei Biomedical Research Center
1. 연구논문 > 1. College of Medicine > Dept. of Life Science
Yonsei Authors
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