NDLI: Lysosome-dependent $Ca^{2+}$ release response to Fas activation in coronary arterial myocytes through NAADP: evidence from CD38 gene knockouts

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhang, Fan Xia, Min Li, Pin-Lan
Description	Country affiliation: United States Author Affiliation: Zhang F ( Dept. of Pharmacology and Toxicology, Virginia Commonwealth Univ., Richmond, 23298, USA.)
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, we found that FasL (10 ng/ml) significantly increased Ca(2+) release from 142.5 +/- 22.5 nM at the basal level to 509.4 +/- 64.3 nM in CD38(+/+) CAMs but not in CD38(-/-) CAMs. However, direct delivery of NAADP, the CD38 metabolite, into CD38(-/-) CAMs still markedly increased Ca(2+) release, which could be significantly attenuated by a lysosomal function inhibitor, bafilomycin A1 (Baf), or a NAADP antagonist, pyridoxalphosphate-6-azophenyl-2-disulfonic acid. Confocal microscopy further demonstrated that FasL produced a typical two-phase Ca(2+) release with a local Ca(2+) burst from lysosomes, followed by a global Ca(2+) response in CD38(+/+) CAMs. In isolated perfused septal coronary arteries from CD38(+/+) mice, FasL was found to significantly increase U-46619-induced vasoconstriction from 29.2 +/- 7.3 to 63.2 +/- 10.3%, which was abolished by Baf (100 nM). These results strongly indicate that the early response of CAMs to FasL is to increase intracellular Ca(2+) levels and enhance the vascular reactivity through stimulation of NAADP production and lysosome-associated two-phase Ca(2+) release in coronary arteries.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
DOI	10.1152/ajpcell.00533.2009
Journal	American Journal of Physiology - Cell Physiology
Issue Number	5
Volume Number	298
Language	English
Publisher	American Physiological Society
Publisher Date	2010-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Antigens, Cd38 Metabolism Antigens, Cd95 Calcium Membrane Glycoproteins Myocytes, Smooth Muscle Analogs & Derivatives 15-hydroxy-11 Alpha,9 Alpha-(epoxymethano)prosta-5,13-dienoic Acid Pharmacology Animals Genetics Coronary Vessels Cytology Fas Ligand Protein Gene Expression Regulation Lysosomes Mice Mice, Knockout Muscle, Smooth, Vascular Vasoconstrictor Agents Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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