C/EBP-α ameliorates CCl(4)-induced liver fibrosis in mice through promoting apoptosis of hepatic stellate cells with little apoptotic effect on hepatocytes in vitro and in vivo

Apoptosis. 2012 May;17(5):492-502. doi: 10.1007/s10495-012-0700-y.

Abstract

CCAAT enhancer binding protein-α (C/EBP-α) is a transcript factor that regulates adipocyte differentiation and induces apoptosis in hepatic stellate cells (HSCs) in vivo and in vitro. However, the effect of C/EBP-α on hepatocytes in vivo remains unknown. This study investigated whether C/EBP-α exerts different apoptotic effects on hepatocytes and HSCs in vitro and in vivo. An adenovirus vector-expressing C/EBP-α gene was constructed, and a rat hepatic stellate cell lines (HSC-T6) and hepatocytes were transfected. A CCl(4)-induced liver fibrosis model in mice was also utilized. C/EBP-α induced apoptosis in hepatocytes and HSCs, but a significant difference between these cell types was observed in vitro. The mitochondrial pathway was involved in the apoptotic process and was predominant in HSC-T6 apoptosis. In the CCl(4)-induced mice liver fibrosis model, the administration of Ad-C/EBP-α decreased extracellular matrix deposition, including collagen and hydroxyproline content, and γ-GT levels, a marker of liver damage, were reduced significantly. Immunohistochemistry and TUNEL assay results showed an increase of apoptosis in HSCs, but hepatocytes were less affected. C/EBP-α induced differential apoptotic effects in hepatocytes and HSCs in vitro and in vivo. This differential effect could be a potential target for the treatment of hepatic fibrosis with little hepatic toxicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Animals
  • Apoptosis*
  • CCAAT-Enhancer-Binding Protein-alpha / biosynthesis
  • CCAAT-Enhancer-Binding Protein-alpha / genetics
  • CCAAT-Enhancer-Binding Protein-alpha / physiology*
  • Carbon Tetrachloride
  • Caspases / genetics
  • Caspases / metabolism
  • Cells, Cultured
  • Collagen / metabolism
  • DNA Fragmentation
  • Extracellular Matrix / metabolism
  • Gene Expression
  • Hepatic Stellate Cells / metabolism
  • Hepatic Stellate Cells / physiology*
  • Hepatocytes / metabolism
  • Hepatocytes / physiology*
  • Hydroxyproline / metabolism
  • Liver Cirrhosis / chemically induced
  • Liver Cirrhosis / metabolism*
  • Liver Cirrhosis / pathology
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Rats
  • Recombinant Proteins / biosynthesis
  • Recombinant Proteins / genetics
  • gamma-Glutamyltransferase / metabolism

Substances

  • Actins
  • CCAAT-Enhancer-Binding Protein-alpha
  • Recombinant Proteins
  • smooth muscle actin, rat
  • Collagen
  • Carbon Tetrachloride
  • gamma-Glutamyltransferase
  • Caspases
  • Hydroxyproline