Effects of very low-density lipoprotein on cellular lipid accumulation and the expression of monocyte chemoattractant protein-1 in human mesangial cells.
- Author:
Jing LI
1
;
Hang LI
;
Yu-Bing WEN
;
Xue-Wang LI
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line; Chemokine CCL2; genetics; metabolism; Humans; Lipoproteins, VLDL; pharmacology; toxicity; Mesangial Cells; cytology; metabolism; RNA, Messenger; genetics; metabolism; Triglycerides; metabolism
- From: Acta Academiae Medicinae Sinicae 2009;31(1):55-59
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo 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.
METHODSAn 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.
RESULTSVLDL 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.
CONCLUSIONSVLDL 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.
