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

Heesang Song; Byoung Keuk Kim; Woochul Chang; Soyeon Lim; Byeong Wook Song; Min Ji Cha; Yangsoo Jang; Ki Chul Hwang

doi:10.3109/10799893.2010.529577

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

Heesang Song, Byoung Keuk Kim, Woochul Chang, Soyeon Lim, Byeong Wook Song, Min Ji Cha, Yangsoo Jang, Ki Chul Hwang

Department of Internal Medicine

Research output: Contribution to journal › Article › peer-review

17 Citations (Scopus)

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 H₂O₂-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 H₂O₂-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 ₂O₂-treated cardiomyocytes were rescued by TG2 silencing. Together, our data strongly suggest that oxidative stress up-regulates TG2 expression in cardiomyocytes, leading to apoptosis.

Original language	English
Pages (from-to)	66-74
Number of pages	9
Journal	Journal of Receptors and Signal Transduction
Volume	31
Issue number	1
DOIs	https://doi.org/10.3109/10799893.2010.529577
Publication status	Published - 2011 Feb

Bibliographical note

Funding Information:
This work was supported by the Korea Research Foundation Grant funded by the Korean Government (MOEHRD, Basic Research Promotion Fund) (KRF-2007-313-E00098) and by a faculty research grant of Yonsei University College of Medicine for 2008.

All Science Journal Classification (ASJC) codes

Biochemistry
Molecular Biology
Cell Biology

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10.3109/10799893.2010.529577

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title = "Tissue transglutaminase 2 promotes apoptosis of rat neonatal cardiomyocytes under oxidative stress",

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 H2O2-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 H2O2-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 2O2-treated cardiomyocytes were rescued by TG2 silencing. Together, our data strongly suggest that oxidative stress up-regulates TG2 expression in cardiomyocytes, leading to apoptosis.",

author = "Heesang Song and Kim, {Byoung Keuk} and Woochul Chang and Soyeon Lim and Song, {Byeong Wook} and Cha, {Min Ji} and Yangsoo Jang and Hwang, {Ki Chul}",

note = "Funding Information: This work was supported by the Korea Research Foundation Grant funded by the Korean Government (MOEHRD, Basic Research Promotion Fund) (KRF-2007-313-E00098) and by a faculty research grant of Yonsei University College of Medicine for 2008.",

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AU - Song, Byeong Wook

AU - Cha, Min Ji

AU - Jang, Yangsoo

AU - Hwang, Ki Chul

N1 - Funding Information: This work was supported by the Korea Research Foundation Grant funded by the Korean Government (MOEHRD, Basic Research Promotion Fund) (KRF-2007-313-E00098) and by a faculty research grant of Yonsei University College of Medicine for 2008.

PY - 2011/2

Y1 - 2011/2

N2 - 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 H2O2-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 H2O2-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 2O2-treated cardiomyocytes were rescued by TG2 silencing. Together, our data strongly suggest that oxidative stress up-regulates TG2 expression in cardiomyocytes, leading to apoptosis.

AB - 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 H2O2-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 H2O2-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 2O2-treated cardiomyocytes were rescued by TG2 silencing. Together, our data strongly suggest that oxidative stress up-regulates TG2 expression in cardiomyocytes, leading to apoptosis.

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

Abstract

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