Abstract
BackgroundTo explore the potential mechanism of inducible co-stimulator (ICOS) inhibition of lipid phagocytosis in human aortic smooth muscle cells (HASMCs).MethodsExcess Dil (1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate)-labeled oxidized low-density lipoprotein (ox-LDL) was used to induce HASMCs to form a foam cell model; HASMCs were cultured together with ICOS-overexpressed JurKat (JK-ICOS) cells or recombinant human ICOS protein (rICOS protein) to be stimulated, and a confocal laser microscope was used to observe the lipid phagocytosis of HASMCs. Reverse transcription quantitative polymerase chain reaction (RT-qPCR), western blot, and immunofluorescence staining were used to detect the expression of the lipid phagocytic receptor, cluster of differentiation 36 (CD36) in HASMCs.ResultsThe uptake of Dil ox-LDL by HASMCs was concentration-dependent, and excessive Dil ox-LDL uptake led to lipid accumulation in HASMCs. Pretreatment with JK-ICOS cells or rICOS protein for HASMCs 48 hours reduced Dil ox-LDL-induced lipid accumulation. Compared with HASMCs co-cultured with empty lentiviral JurKat (JK-EV) cells, the messenger RNA (mRNA) and protein expressions of CD36 in HASMCs co-cultured with JK-ICOS cells were significantly down-regulated. The results of immunofluorescence staining showed that co-culturing with JK-ICOS cells could down-regulate ox-LDL-induced expression of CD36 in HASMCs, but JK-EV cells could not. Similarly, the results of qPCR, western blot, and immunofluorescence staining showed that rICOS protein could down-regulate the ox-LDL-induced expression of CD36 in HASMCs, but this down-regulation was not as significant as that in JK-ICOS cells.ConclusionsICOS could inhibit the lipid phagocytosis of HASMCs by down-regulating the expression of CD36, suggesting a potential anti-atherosclerosis (anti-AS) mechanism of ICOS, and preventing ox-LDL-induced formation of myogenic foam cells.
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