Differentially expressed genes identified by microarray analysis following leptin treatment of hepatic stellate cells.
- Author:
Li-hua ZHONG
1
;
Jun CHENG
;
Li-ying ZHU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cells, Cultured; Gene Expression Profiling; Hepatic Stellate Cells; drug effects; metabolism; Leptin; pharmacology; Oligonucleotide Array Sequence Analysis; methods; Pulmonary Surfactant-Associated Protein A; genetics; Rats; Stearoyl-CoA Desaturase; genetics
- From: Chinese Medical Journal 2010;123(6):726-729
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDLiver fibrosis is the process through which numerous chronic liver diseases develop into liver cirrhosis. Leptin can activate hepatic stellate cells (HSCs) and play an important role in the formation of liver fibrosis. However, the process by which leptin activates HSCs is complicated, and research on this process is limited. The aim of this study was to explore the related changes in gene expression and the control mechanisms involved in leptin activated HSCs to understand the overall mechanism of liver fibrosis development.
METHODSWe cultivate rat HSCs, with and without stimulation by leptin, and extracted mRNA. Differentially expressed genes were detected by microarray analysis.
RESULTSThe differentially expressed genes identified included six upregulated genes and six downregulated genes. The representative upregulated genes included short chain dehydrogenase (CY5/CY3 = 2.265) and pulmonary surfactant protein A1 (CY5/CY3 = 2.036). The significant downregulated gene encoded hepatic stearoyl coenzyme A desaturase 1 (SCD-1) (CY5/CY3 = 0.351).
CONCLUSIONLeptin might mediate the molecular biological mechanisms of liver fibrosis.
