RGD Reference Report - Carbon monoxide inhibition of apoptosis during ischemia-reperfusion lung injury is dependent on the p38 mitogen-activated protein kinase pathway and involves caspase 3. - Rat Genome Database

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Carbon monoxide inhibition of apoptosis during ischemia-reperfusion lung injury is dependent on the p38 mitogen-activated protein kinase pathway and involves caspase 3.

Authors: Zhang, X  Shan, P  Otterbein, LE  Alam, J  Flavell, RA  Davis, RJ  Choi, AM  Lee, PJ 
Citation: Zhang X, etal., J Biol Chem 2003 Jan 10;278(2):1248-58.
RGD ID: 634700
Pubmed: PMID:12399465   (View Abstract at PubMed)
DOI: DOI:10.1074/jbc.M208419200   (Journal Full-text)

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 to minimal levels of CO inhibits apoptosis and enhances phospho-p38 mitogen-activated protein kinase (MAPK) activation in A-R. Transfection of p38alpha dominant negative mutant 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 I-R injury 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.



Objects referenced in this article
Gene Casp3 caspase 3 Rattus norvegicus
Gene Mapk14 mitogen activated protein kinase 14 Rattus norvegicus

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