ArticleAmerican journal of physiology. Cell physiology2010
Lysosome-dependent Ca(2+) release response to Fas activation in coronary arterial myocytes through NAADP: evidence from CD38 gene knockouts.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- CD38 connects the heart and brain.Translational psychiatry · 2025Review
- Bafilomycin A1 Molecular Effect on ATPase Activity of Subcellular Fraction of Human Colorectal Cancer and Rat Liver.International journal of molecular sciences · 2024Article
- Enzymology of CaCells · 2023Review
- NAADP-Mediated CaHandbook of experimental pharmacology · 2023Article
- Regulation of exosome release by lysosomal acid ceramidase in coronary arterial endothelial cells: Role of TRPML1 channel.Current topics in membranes · 2022Article
- Regulation of TRPML1 channel activity and inflammatory exosome release by endogenously produced reactive oxygen species in mouse podocytes.Redox biology · 2021Article
- Abnormal podocyte TRPML1 channel activity and exosome release in mice with podocyte-specific Asah1 gene deletion.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2021Article
- Lysosomal TRPML1 Channel: Implications in Cardiovascular and Kidney Diseases.Advances in experimental medicine and biology · 2021Article
- Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases.International journal of molecular sciences · 2020Review
- NAADP Receptors.Cold Spring Harbor perspectives in biology · 2019Review
- Control of lysosomal TRPML1 channel activity and exosome release by acid ceramidase in mouse podocytes.American journal of physiology. Cell physiology · 2019Article
- Lysosomal cholesterol accumulation in macrophages leading to coronary atherosclerosis in CD38(-/-) mice.Journal of cellular and molecular medicine · 2016Article
- Preferential Coupling of the NAADP Pathway to Exocytosis in T-Cells.Messenger (Los Angeles, Calif. : Print) · 2015Article
- Contribution of Nrf2 to Atherogenic Phenotype Switching of Coronary Arterial Smooth Muscle Cells Lacking CD38 Gene.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2015Article
- Concentration-Dependent Diversifcation Effects of Free Cholesterol Loading on Macrophage Viability and Polarization.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2015Article
- Enhancement of dynein-mediated autophagosome trafficking and autophagy maturation by ROS in mouse coronary arterial myocytes.Journal of cellular and molecular medicine · 2014Article
- Defective autophagosome trafficking contributes to impaired autophagic flux in coronary arterial myocytes lacking CD38 gene.Cardiovascular research · 2014Article
- Regulation of autophagic flux by dynein-mediated autophagosomes trafficking in mouse coronary arterial myocytes.Biochimica et biophysica acta · 2013Article
- Autophagy maturation associated with CD38-mediated regulation of lysosome function in mouse glomerular podocytes.Journal of cellular and molecular medicine · 2013Article
- Effect of aging on calcium signaling in C57Bl6J mouse cerebral arteries.Pflugers Archiv : European journal of physiology · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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.
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