Modulation of Endothelial Cell Apoptosis by Heme Oxygenase-1-Derived Carbon Monoxide
- 1 April 2002
- journal article
- review article
- Published by Mary Ann Liebert Inc in Antioxidants and Redox Signaling
- Vol. 4 (2) , 321-329
- https://doi.org/10.1089/152308602753666370
Abstract
It is well established that expression of heme oxygenase-1 (HO-1) acts in a cytoprotective manner in a variety of cell types, including in endothelial cells (EC). We have recently shown that HO-1 expression protects EC from undergoing apoptosis. We have also shown that the antiapoptotic effect of HO-1 is mediated through heme catabolism into the gas carbon monoxide (CO). In this review, we discuss the possible molecular mechanisms by which HO-1-derived CO suppresses EC apoptosis. We will review data suggesting that the antiapoptotic effect of CO acts through the activation of the p38 mitogen-activated protein kinase signal transduction pathway and requires the activation of the transcription factor nuclear factor-κB (NF-κB), as well as the expression of a subset of NF-κB-dependent antiapoptotic genes.Keywords
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