Role of PPARγ/CD36 signaling pathway in macrophage lipid metabolism after Mycobacterium tuberculosis infection / 中华微生物学和免疫学杂志
Chinese Journal of Microbiology and Immunology
;
(12): 749-756, 2021.
Article
in Chinese
| WPRIM
| ID: wpr-912109
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Language:
Chinese
Journal:
Chinese Journal of Microbiology and Immunology
Year:
2021
Type:
Article
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