The Role of Renal Cell CD36 in Inflammatory Factor-Induced Fatty Acid Uptake and Lipid Deposition
WEI Li, WU Tingting, CHEN Yaxi, YANG Ping*
Chronic inflammation and lipid metabolism disorder are important features of chronic kidney disease. The mechanism of how inflammatory factors affect lipid metabolism in renal cells is not clear. This study aims to explore whether inflammatory factors promote fatty acid uptake and lipid deposition in renal cells by up-regulating the expression of fatty acid transporter CD36. First, HMCs and HK2 cells were treated by TNF-α (tumor necrosis factor-α) and IL-6 (interleukin-6) respectively for 24 h. TG (triglycerides) were detected by enzymatic detection. The mRNA expression level of CD36 was detected the by qRT-PCR. Next, CD36 overexpression cell model was established, fatty acids was fluorescent labeled to observe the uptake rate the of exogenous fatty acids. Then, small RNA interference technique was used to construct a cell model with low expression of CD36. Intracellular TG, intracellular FFA (free fatty acid), GRP78 (glucose regulated protein 78) and IRE1 (inosital-requiring enzyme 1) mRNA expression level were detected respectively. The results showed TNF-α and IL-6 promoted the accumulation of TG in HMCs and HK2 cells and stimulate the expression of CD36. Meanwhile, CD36 overexpression promoted FFA uptake in HMCs and HK2 cells. When CD36 expression was interfered, accumulation of TG and FFA, uptake rate of FFA and ERS (endoplasmic reticulum stress) induced by inflammatory cytokines were inhibited. In conclusion, inflammatory cytokines promotes CD36 expression in HMCs and HK2 cells, leading to increased uptake of FFA and lipid accumulation. Inhibition of CD36 expression may alleviate lipid accumulation and ERS induced by inflammatory cytokines. These results suggest that CD36 may be a potential therapeutic target for chronic renal disease.
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