CGMP increases antioxidant function and attenuates oxidant cell death in mouse lung microvascular endothelial cells by a protein kinase G-dependent mechanism.

ABSTRACT: Increasing evidence suggests that endothelial cytotoxicity from reactive oxygen species (ROS) contributes to the pathogenesis of acute lung injury. Treatments designed to increase intracellular cGMP attenuate ROS-mediated apoptosis and necrosis in several cell types, but the mechanisms are not understood, and the effect of cGMP on pulmonary endothelial cell death remains controversial. In the current study, increasing intracellular cGMP by either 8pCPT-cGMP (50 microM) or atrial natriuretic peptide (10 nM) significantly attenuated cell death in H(2)O(2)-challenged mouse lung microvascular (MLMVEC) monolayers. 8pCPT-cGMP also decreased perfusate LDH release in isolated mouse lungs exposed to H(2)O(2) or ischemia-reperfusion. The protective effect of increasing cGMP in MLMVECs was accompanie

SUBMITTER: Stephens RS 

PROVIDER: S-EPMC2951066 | biostudies-literature | 2010 Sep

REPOSITORIES: biostudies-literature