Lysosome-dependent Ca(2+) release response to Fas activation in coronary arterial myocytes through NAADP: evidence from CD38 gene knockouts.

ABSTRACT: Activation of the death receptor Fas has been implicated in the development of vascular injury or disease, but most studies have focused on its role in the regulation of cell apoptosis and growth. The present study was designed to examine the early response of coronary artery to Fas activation by its ligand, FasL. The hypothesis being tested is that CD38 signaling pathway mediates FasL-induced intracellular Ca(2+) release through nicotinic acid adenine dinucleotide phosphate (NAADP) in mouse coronary arterial myocytes (CAMs) and thereby produces vasoconstriction in coronary arteries. HPLC analysis demonstrated that FasL markedly increased NAADP production in CAMs from wild-type mice (CD38(+/+)) but not in cells from CD38 knockout (CD38(-/-)) mice. Using fluorescent Ca(2+) imaging analysis,

SUBMITTER: Zhang F 

PROVIDER: S-EPMC2867387 | biostudies-literature | 2010 May

REPOSITORIES: biostudies-literature