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Antifibrotic effect of globular adiponectin in human hepatocyte
Author(s) -
Huh Joo Young,
Ha Hunjoo
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.978.11
Subject(s) - adiponectin , endocrinology , medicine , cirrhosis , extracellular matrix , hepatic stellate cell , fibrosis , adiponectin receptor 1 , receptor , downregulation and upregulation , adipose tissue , fibronectin , chemistry , hepatocyte , insulin , insulin resistance , biochemistry , in vitro , gene
Adiponectin is a secreted 30‐kDa protein, which is mainly produced by adipose tissue. Adiponectin exhibits insulin‐sensitizing metabolic effects and anti‐atherogenic effects through its receptors (adiponectin receptor 1 and 2). Hypoadiponectinemia has recently been reported in liver cirrhosis. Further, adiponectin receptor 2, but not receptor 1, expression was decreased during the development of liver fibrosis. There is increasing evidence that hepatocytes in addition to stellate cells may play an important role in the development and progression of liver fibrosis. Thus, the objective of the present study was to determine the direct effect of adiponectin on extracellular matrix (ECM) protein expression of HepG2 cells as a first step to investigate the role of adiponectin in liver fibrosis. HepG2 cells were incubated with 10 ng/mL TGF‐β1 in the presence of globular adiponectin (0‐5 μg/mL) for up to 48 hours. TGF‐β1 significantly increased fibronectin, collagen I, and collagen IV mRNA and protein expression. Globular adiponectin inhibited TGF‐β1‐induced ECM upregulation in a dose‐dependent manner. These results suggest that adiponectin may provide a novel therapeutic strategy for the attenuation of liver fibrosis. (Supported by R01‐2006‐000‐10829‐0 and R15‐2006‐020 from KOSEF and BK 21)