Role of PPARγ/CD36 signaling pathway in macrophage lipid metabolism after Mycobacterium tuberculosis infection
10.3760/cma.j.cn112309-20201231-00578
- VernacularTitle:PPARγ/CD36信号通路在结核分枝杆菌感染巨噬细胞脂质代谢中的作用
- Author:
DongMei LIU
1
;
Xiaoqun HAN
;
Jing YANG
;
Qin DENG
;
Haili WANG
;
Xiaojie ZHAO
Author Information
1. 宜春学院化学与生物工程学院 336000
- Keywords:
Mycobacterium tuberculosis;
PPARγ;
CD36;
Macrophage;
Lipid metabolism
- From:
Chinese Journal of Microbiology and Immunology
2021;41(10):749-756
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the role of peroxisome proliferator-activated receptor γ (PPARγ)/CD36 signaling pathway in macrophage lipid metabolism after Mycobacterium tuberculosis ( Mtb) infection. Methods:THP-1-derived macrophages were infected with Mtb. Four groups were included in this study, which were control group, Mtb infection group, Mtb+ rosiglitazone (ROZ, PPARγ agonist) group and Mtb+ GW9662 (PPARγ antagonist) group. Western blot and RT-PCR were used to detect the expression of PPARγ in macrophages at protein and mRNA levels, respectively. The lipids in cells were detected by oil red O staining. The concentrations of total cholesterol (TC), triglycerides (TG), low density lipoprotein (LDL-C) and high density lipoprotein (HDL-C) in the supernatant of cell culture were detected by automatic biochemical analyzer. The expression of CD36 was detected by immunohistochemistry. CCK-8 was used to detect the proliferation rate of macrophages. Results:Mtb infection significantly increased the expression of PPARγ in macrophages ( P<0.001), promoted intracellular lipid aggregation and CD36 expression and decreased the levels of TC, TG, LDL-C and HDL-C in the supernatant of cell culture ( P<0.001) and cell proliferation rate ( P<0.001). PPARγ agonist significantly enhanced the intracellular lipid accumulation and CD36 expression that were induced by Mtb infection and down-regulated the lipid level in the supernatant of cell culture and cell proliferation rate, while PPARγ antagonist reversed the above effects. Conclusions:PPARγ played a role in lipid metabolism in Mtb-infected macrophages through affecting CD36 expression.
