Key result
Id1 expression triggers cardiomyocyte apoptosis via mitochondrial reactive oxygen species.
Why the study?
The mechanism by which Id1 expression affects cardiac myocyte viability and induces apoptosis was unclear.
Id1 expression induces apoptosis in cardiac myocytes via a redox-dependent mechanism involving mitochondrial reactive oxygen species.
Id1 induces myocyte apoptosis in vitro; leaves open its role in cardiac remodeling or failure.
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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Tanaka et al. (1998) studied this question. Expression of Id1 via recombinant adenovirus (Ad.Id1) was evaluated on Apoptosis and cell viability. Expression of Id1 in cardiac myocytes resulted in apoptosis through a redox-dependent mechanism involving mitochondrial reactive oxygen species.
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