Interference of S100A16 suppresses lipid accumulation and inflammation in high glucose-induced HK-2 cells
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Updated: Nov 23, 2025
Measurement of Fatty Acid β-Oxidation in a Suspension of Freshly Isolated Mouse Hepatocytes
Published on: September 9, 2021
1Department of Nephrology, Zhangzhou Affiliated Hospital of Fujian Medical University, NO. 59 Shengli Road, Xiangcheng District, Zhangzhou, 363000, Fujian, China. 18006062616@189.cn.
Purpose:
Diabetic nephropathy (DN) is a major complication of diabetic mellitus and usually leads to the end-stage renal disease. Inflammation-induced lipid disorders have been proposed to play an important role in the pathogenesis of DN. S100A16 is a novel adipogenic factor, but has not been investigated in DN. This study aims to explore the role of S100A16 in high glucose (HG)-induced HK-2 cells.
Methods:
CCK-8 assay was used to detect cell viability. Cell transfection was performed to knockdown S100A16. Oil red staining was performed to assay lipid accumulation. qRT-PCR and western blotting were conducted to examine corresponding gene expression. Intracellular cholesterol was determined by enzymatic assay. Inflammatory cytokines production was measured using ELISA kits.
Results:
The results exhibited lipid accumulation and upregulation of S100A16 in HG-induced HK-2 cells. S100A16 knockdown significantly reduced lipid droplets and cholesterol, and decreased the production of inflammatory cytokines induced by HG. Besides, S100A16 knockdown decreased the expression of SCAP, SREBP1, SCD1 and SCAP. However, the inhibitory effect in HG-induced HK-2 cells made by S100A16 was reversed by SREBP1 overexpression.
Conclusion:
These results suggested that S100A16 knockdown might protect against HG-induced lipid accumulation and inflammation in HK-2 cells through regulating SCAP/SREBP1 signaling.
