Interleukin-6 protects hepatocytes from CCl4-mediated necrosis and apoptosis in mice by reducing MMP-2 expression

J Hepatol. 2005 Apr;42(4):548-56. doi: 10.1016/j.jhep.2004.11.043.

Abstract

Background/aims: Interleukin-6 stimulates liver regeneration and promotes hepatoprotection following experimental liver injury, but underlying mechanisms have not been fully characterized. Because studies suggest matrix metalloproteinase-2 (MMP-2) may promote liver injury, we examined whether IL-6 exerted its protective effects via regulation of MMP-2.

Methods: MMP-2 was analyzed in livers of IL-6-/- and IL-6+/+ mice following CCl(4) administration. IL-6-/- mice were pretreated with IL-6 and liver histology and MMP-2 expression were examined after liver injury. IL-6-/- mice were treated with an MMP-2 inhibitor and assessment of injury (histology and serum ALT levels), apoptosis by TUNEL assay, and hepatocyte proliferation by BRDU-labeling was performed. These studies were complemented by analysis of cultured stellate cells.

Results: MMP-2 mRNA, protein, and activity was increased in IL-6-/- livers. Restoration of IL-6 signaling in IL-6-/- mice rescued injury and restored MMP-2 expression to wild-type levels. Furthermore, pharmacologic inhibition of MMP-2 decreased hepatocellular injury and apoptosis in IL-6-/- mice. In cultured stellate cells, recombinant IL-6 suppressed endogenous MMP-2 mRNA and protein expression.

Conclusions: IL-6 may be hepatoprotective in acute injury through down-regulation of MMP-2. These findings suggest a role for MMP-2 in amplifying liver injury in vivo.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acute Disease
  • Animals
  • Apoptosis
  • Carbon Tetrachloride
  • Chemical and Drug Induced Liver Injury / pathology
  • Chemical and Drug Induced Liver Injury / physiopathology
  • Enzyme Inhibitors / pharmacology
  • Hepatocytes / enzymology*
  • Hepatocytes / pathology
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism*
  • Liver Cirrhosis / pathology*
  • Liver Cirrhosis / physiopathology*
  • Matrix Metalloproteinase 2 / genetics
  • Matrix Metalloproteinase 2 / metabolism*
  • Matrix Metalloproteinase Inhibitors
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Necrosis
  • RNA, Messenger / analysis
  • Signal Transduction / physiology

Substances

  • Enzyme Inhibitors
  • Interleukin-6
  • Matrix Metalloproteinase Inhibitors
  • RNA, Messenger
  • Carbon Tetrachloride
  • Matrix Metalloproteinase 2