dimethylarginine and Acute-Lung-Injury

The molecular mechanisms by which the endothelial barrier becomes compromised during lipopolysaccharide (LPS) mediated acute lung injury (ALI) are still unresolved. We have previously reported that the disruption of the endothelial barrier is due, at least in part, to the uncoupling of endothelial nitric oxide synthase (eNOS) and increased peroxynitrite-mediated nitration of RhoA. The purpose of this study was to elucidate the molecular mechanisms by which LPS induces eNOS uncoupling during ALI. Exposure of pulmonary endothelial cells (PAEC) to LPS increased pp60

Topics: Acute Lung Injury; Amidohydrolases; Animals; Arginine; Endothelial Cells; Gene Expression Regulation; Lipopolysaccharides; Mice; Mitochondria; Mutation; Nitric Oxide; Nitric Oxide Synthase Type III; Peroxynitrous Acid; Phosphorylation; Proto-Oncogene Proteins pp60(c-src); Superoxides