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Expression of Id1 Results in Apoptosis of Cardiac Myocytes through a Redox-dependent Mechanism
Journal article   Open access   Peer reviewed

Expression of Id1 Results in Apoptosis of Cardiac Myocytes through a Redox-dependent Mechanism

Koichi Tanaka, John B Pracyk, Kazuyo Takeda, Zu-Xi Yu, Victor J Ferrans, Shailesh S Deshpande, Michitaka Ozaki, Paul M Hwang, Charles J Lowenstein, Kaikobad Irani, …
The Journal of biological chemistry, Vol.273(40), pp.25922-25928
10/1998
DOI: 10.1074/jbc.273.40.25922
PMID: 9748268
url
https://doi.org/10.1074/jbc.273.40.25922View
Published (Version of record) Open Access

Abstract

We have constructed a recombinant adenovirus (Ad.Id1) that allows for efficient expression of the helix-loop-helix protein Id1. After infection with Ad.Id1, neonatal cardiac myocytes display a significant reduction in viability, which was proportional to the level of Id1 expression. A similar effect was observed in adult myocytes. Morphological and biochemical assays demonstrated that Id1 expression resulted in myocyte apoptosis. In contrast, expression of Id1 in endothelial cells, vascular smooth muscle cells, or fibroblasts did not affect the viability of these cells. Along with the induction of apoptosis, the expression of Id1 in neonatal cardiac myocytes resulted in an increase in the level of intracellular reactive oxygen species. The source of these reactive oxygen species appears to be the mitochondria. Reducing the ambient oxygen concentration or treatment with a cell-permeant H2O2 scavenger prevented Id1-stimulated apoptosis in cardiac myocytes. These results suggest that the expression of Id1 leads to the induction of apoptosis in cardiac myocytes through a redox-dependent mechanism.

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