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【論文摘要】Endoplasmic Reticulum Stress Related Genes and the Foam Cell Formation
摘要
Background/Synopsis: Endoplasmic reticulum (ER) stress disturbs cholesterol metabolism in human cells by impairing cholesterol synthesis and cholesterol efflux. Cholesterol loading of human monocyte-derived macrophages by modified low-density lipoproteins (LDL) resulted in increased chemokine (C-X-C motif) ligand 8 (CXCL8) and eukaryotic translation initiation factor 2-alpha kinase 3 (EIF2AK3 or PERK) mRNA expressions. Objectives/Purpose: In this study, our aim was to evaluate the role of EIF2AK3 and CXCL8 genes in cellular cholesterol accumulation mediated by modified (desialylated, acetylated, oxidized) LDL. Methods/Results: CD14+ monocytes were isolated from PBMC by positive selection using a MACS system from the blood of healthy donors. Intracellular cholesterol accumulation was induced by incubation of cultured macrophages with native and modified (desialylated, acetylated, oxidized) LDL. Cholesterol accumulation was evaluated in monocyte-derived human macrophages with genes knocked-downed by siRNA for either PERK or CXCL8. The role of genes in cholesterol accumulation was elucidated by computational analysis. Knock-down of CXCL8 and EIF2AK3 (PERK) genes prevented cholesterol accumulation in primary human macrophages after incubation with modified LDL. It is known that CXCL8 and EIF2AK3 are inflammation-related genes. They are also involved in ER stress and in inflammation responses through the PERK/eIF2α/ATF4/CHOP pathway. Our results assumed that ER stress may play a role in cholesterol metabolism in human macrophages. This is a piece of additional evidence that ER stress of macrophages may play a role in atherosclerosis. Based on our data we can propose that the role of ER stress in atherosclerosis is at least related to lipid metabolism and inflammation. Conclusion: Endoplasmic reticulum stress apparently plays a role in foam cell formation.
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