Prostaglandin E2 inhibits transforming growth factor beta 1-mediated induction of collagen alpha 1(I) in hepatic stellate cells

J Hepatol. 2004 Aug;41(2):251-8. doi: 10.1016/j.jhep.2004.04.033.

Abstract

Background/aims: Cyclooxygenase-2 (COX-2) has been implicated in a number of hepatic stellate cell (HSC) functions but its relationship to transforming growth factor-beta 1 (TGF-beta 1)-mediated fibrogenesis is unknown. We assessed the impact of COX-2 inhibition and PGE(2) on the regulation of TGF-beta 1-stimulated matrix synthesis in an immortalized human HSC line, LX-1 and corroborated these findings in primary stellate cells.

Methods: Expression of COX-2 was assessed by Western blotting and real time quantitative PCR. The effect of NS398, a selective COX-2 inhibitor, and PGE(2) on TGF-beta 1-mediated fibrogenesis was examined by measuring mRNA levels of collagen alpha1(I). PGE(2) receptor expression was analyzed by RT-PCR.

Results: Under basal conditions, NS398 suppressed PGE(2) synthesis and induced collagen alpha 1(I) whereas exogenous PGE(2) suppressed expression of collagen alpha1(I). TGF-beta 1 induced COX-2 mRNA, COX-2 protein and PGE(2) biosynthesis. Importantly, TGF-beta 1-mediated induction of collagen alpha 1(I) was markedly suppressed by the addition of exogenous PGE(2). All four major PGE(2) receptors were expressed in LX-1 cells.

Conclusions: These results suggest that COX-2-derived PGE(2) inhibits both basal and TGF-beta 1-mediated induction of collagen synthesis by HSC. Based on these findings, it will be important to determine whether inhibiting COX-derived PGE(2) synthesis alters the progression of liver fibrosis in vivo.

Publication types

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

MeSH terms

  • Animals
  • Cell Line, Transformed
  • Collagen Type I / antagonists & inhibitors
  • Collagen Type I / biosynthesis*
  • Collagen Type I, alpha 1 Chain
  • Cyclooxygenase 2
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors / pharmacology
  • DNA-Binding Proteins / genetics
  • Dinoprostone / biosynthesis
  • Dinoprostone / pharmacology
  • Dinoprostone / physiology*
  • Heat-Shock Proteins / antagonists & inhibitors
  • Humans
  • Isoenzymes / biosynthesis
  • Isoenzymes / metabolism
  • Liver / cytology*
  • Liver / drug effects
  • Liver / enzymology
  • Liver / metabolism*
  • Membrane Proteins
  • Nitrobenzenes / pharmacology
  • Prostaglandin-Endoperoxide Synthases / biosynthesis
  • Prostaglandin-Endoperoxide Synthases / metabolism
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Prostaglandin E / metabolism
  • Serpins
  • Smad Proteins
  • Sulfonamides / pharmacology
  • Trans-Activators / genetics
  • Transforming Growth Factor beta / pharmacology
  • Transforming Growth Factor beta / physiology*
  • Transforming Growth Factor beta1

Substances

  • Collagen Type I
  • Collagen Type I, alpha 1 Chain
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors
  • DNA-Binding Proteins
  • Heat-Shock Proteins
  • Isoenzymes
  • Membrane Proteins
  • Nitrobenzenes
  • RNA, Messenger
  • Receptors, Prostaglandin E
  • Serpins
  • Smad Proteins
  • Sulfonamides
  • TGFB1 protein, human
  • Tgfb1 protein, rat
  • Trans-Activators
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1
  • N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases
  • Dinoprostone