Regulatory mechanisms of C4b-binding protein (C4BP)alpha and beta expression in rat hepatocytes by lipopolysaccharide and interleukin-6

J Thromb Haemost. 2008 Nov;6(11):1858-67. doi: 10.1111/j.1538-7836.2008.03129.x. Epub 2008 Aug 22.

Abstract

Background: C4b-binding protein (C4BP), a multimeric protein structurally composed of alpha chains (C4BPalpha) and a beta chain (C4BPbeta), regulates the anticoagulant activity of protein S (PS). Patients with sepsis have increased levels of plasma C4BP, which appears to be induced by interleukin (IL)-6. However, it is not fully understood how lipopolysaccharide (LPS) and IL-6 affect the plasma C4BP antigen level and C4BPalpha and C4BPbeta expression in hepatocytes.

Objectives: To assess the effect of LPS and IL-6 on plasma C4BP, PS-C4BP complex levels, PS activity, and C4BP expression by rat liver in vivo and on C4BP expression by isolated rat hepatocytes in vitro.

Results: Plasma C4BP antigen level transiently decreased from 2 to 12 h after LPS (2 mg kg(-1)) injection, and then it abruptly increased up to 24 h after LPS injection. Plasma C4BP antigen level increased until 8 h after IL-6 (10 microg kg(-1)) injection, and then gradually decreased up to 24 h after IL-6 injection. LPS significantly decreased the protein and mRNA expression of both C4BPalpha and C4BPbeta in rat hepatocytes, and this effect was inhibited by NFkappaB and MEK/ERK inhibitors. IL-6 mediated increase in C4BPbeta expression in rat hepatocytes, which leads to increased plasma PS-C4BP complex level and to decreased plasma PS activity, was inhibited by inhibition of STAT-3.

Conclusion: LPS decreases both C4BPalpha and C4BPbeta expression via the NFkappaB and MEK/ERK pathways, whereas IL-6 specifically increases C4BPbeta expression via the STAT-3 pathway, causing an increase in plasma PS-C4BP complex, and thus decreasing the anticoagulant activity of PS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Complement C4b-Binding Protein / analysis*
  • Complement C4b-Binding Protein / genetics
  • Hepatocytes / metabolism*
  • Interleukin-6 / pharmacology*
  • Kinetics
  • Lipopolysaccharides / pharmacology*
  • Liver / metabolism
  • Mitogen-Activated Protein Kinases
  • NF-kappa B
  • Protein S / metabolism*
  • RNA, Messenger / analysis
  • Rats
  • STAT3 Transcription Factor

Substances

  • Complement C4b-Binding Protein
  • Interleukin-6
  • Lipopolysaccharides
  • NF-kappa B
  • Protein S
  • RNA, Messenger
  • STAT3 Transcription Factor
  • Mitogen-Activated Protein Kinases