[Effects of very low-density lipoprotein on cellular lipid accumulation and the expression of monocyte chemoattractant protein-1 in human mesangial cells]

Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2009 Feb;31(1):55-9.
[Article in Chinese]

Abstract

Objective: To investigate the effects of very low-density lipoprotein (VLDL) on cellular lipid accumulation and the expression of monocyte chemoattractant protein-1 (MCP-1) in human mesangial cells.

Methods: An established stable human mesangial cell line (HMCL) was used in all experiments. VLDL-induced cellular lipid deposition was visualized by Oil Red O staining and analyzed quantitatively by standard enzymatic procedures. MCP-1 mRNA and protein expression levels in treated HMCLs were determined by real-time quantitative RT-PCR and enzyme-linked immunosorbent assay, respectively. For adhesion study, HMCLs were treated with VLDL for 12 hours, followed by a one-hour incubation with THP-1 cells.

Results: VLDL induced cellular lipid accumulation in HMCLs in a time- (0-24 h) and dose- (0-200 microg/ml) dependent manner, and the principal component of accumulated lipid is triglyceride. In HMCLs, MCP-1 mRNA expression was promoted by VLDL in a time- (0-6 h) and dose- (0-100 microg/ml) dependent manner, and VLDL also enhanced MCP-1 secretion in a dose-dependent manner. Such an effect was accompanied by increased adhesion of monocytes to HMCLs.

Conclusions: VLDL can induce cellular triglyceride accumulation and upregulate the expression of MCP-1 in human mesangial cells. Hence, VLDL may be involved in the pathogenesis of lipid-mediated renal injury.

Publication types

  • English Abstract

MeSH terms

  • Cell Line
  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / metabolism*
  • Humans
  • Lipoproteins, VLDL / pharmacology
  • Lipoproteins, VLDL / toxicity*
  • Mesangial Cells / cytology
  • Mesangial Cells / metabolism*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Triglycerides / metabolism*

Substances

  • CCL2 protein, human
  • Chemokine CCL2
  • Lipoproteins, VLDL
  • RNA, Messenger
  • Triglycerides