Lysosomal cholesterol accumulation in macrophages leading to coronary atherosclerosis in CD38(-/-) mice.

ABSTRACT: The disruption in transportation of oxLDL-derived cholesterol and the subsequent lipid accumulation in macrophages are the hallmark events in atherogenesis. Our recent studies demonstrated that lysosomal Ca(2+) messenger of nicotinic acid adenine dinucleotide phosphate (NAADP), an enzymatic product of CD38 ADP-ribosylcyclase (CD38), promoted lipid endocytic trafficking in human fibroblast cells. The current studies are designed to examine the functional role of CD38/NAADP pathway in the regulation of lysosomal cholesterol efflux in atherosclerosis. Oil red O staining showed that oxLDL concentration-dependently increased lipid buildup in bone marrow-derived macrophages from both wild type and CD38(-/-) , but to a significant higher extent with CD38 gene deletion. Bodipy 493/503 fluorescence

SUBMITTER: Xu X 

PROVIDER: S-EPMC4882979 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature