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

Pub. Date : 2010 May

PMID : 20200208






4 Functional Relationships(s)
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1 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. NAADP Fas ligand (TNF superfamily, member 6) Mus musculus
2 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. NAADP Fas ligand (TNF superfamily, member 6) Mus musculus
3 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. NAADP Fas ligand (TNF superfamily, member 6) Mus musculus
4 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. NAADP Fas ligand (TNF superfamily, member 6) Mus musculus