ArticleJournal of thoracic disease2022
Inducible co-stimulator inhibits lipid phagocytosis of human aortic smooth muscle cells by down-regulating CD36 expression.
Article in Journal of thoracic disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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4 authors at 2 institutions in 1 country.
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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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