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Papers In Press, published online ahead of print October 23, 2002
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520
Corresponding Author: patty.lee{at}yale.edu
Carbon monoxide (CO), a reaction product of the cytoprotective gene heme oxygenase, has been shown to be protective against organ injury in a variety of models. One potential mechanism whereby CO affords cytoprotection is through its anti-apoptotic properties. Our studies show that low-level, exogenous CO attenuates anoxia-reoxygenation (A-R)-induced lung endothelial cell apoptosis. Exposure of primary rat pulmonary artery endothelial cells (PAECs) to minimal levels of CO inhibits apoptosis and enhances phospho-p38 MAPK activation in A-R. Transfection of p38 dominant negative mutant (DNM) or inhibition of p38 MAPK activity with SB203580 ablates the anti-apoptotic effects of CO in A-R. CO, through p38 MAPK, indirectly modulates caspase 3. Furthermore, we correlate our in vitro apoptosis model with an in vivo model of A-R by showing that CO can attenuate ischemia-reperfusion (I-R) of the lung. Taken together, our data are the first to demonstrate in models of A-R that the anti-apoptotic effects of CO are via modulation of p38 MAPK and caspase 3.
J. Biol. Chem, 10.1074/jbc.M208419200
Submitted on August 17, 2002
Revised on October 1, 2002
Accepted on October 23, 2002
Carbon monoxide inhibition of apoptosis during ischemia-reperfusion lung injury is dependent on the p38 mitogen activated protein kinase pathway and involves caspase 3
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