DDAH1 regulates apoptosis and angiogenesis in human fetal pulmonary microvascular endothelial cells.

ABSTRACT: Nitric Oxide (NO) is an endogenous pulmonary vasodilator produced by endothelial NO synthase (eNOS). Asymmetric dimethyl L-arginine (ADMA) is an endogenous inhibitor of eNOS activity. In endothelial cells, ADMA is hydrolyzed to L-citrulline primarily by dimethylarginine dimethyl-aminohydrolase-1 (DDAH1). We tested the hypothesis that DDAH1 expression is essential for maintaining NO production in human fetal pulmonary microvascular endothelial cells (hfPMVEC), such that knockdown of DDAH1 expression will lead to decreased NO production resulting in less caspase-3 activation and less tube formation. We found that hfPMVEC transfected with DDAH1 siRNA had lower NO production than control, with no difference in eNOS protein levels between groups. hfPMVEC transfected with DDAH1 siRNA had lower p

SUBMITTER: Trittmann JK 

PROVIDER: S-EPMC6579941 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature