Transforming growth factors beta1, beta2 and beta3 and their receptors are differentially expressed in human peritoneal fibroblasts in response to hypoxia

Am J Reprod Immunol. 2002 Dec;48(6):387-93. doi: 10.1034/j.1600-0897.2002.01090.x.

Abstract

Problem: Little is known about the role of peritoneal fibroblasts in adhesion formation. This study determines the effect of hypoxia and transforming growth factor (TGF)-beta1 treatment on the expression of TGF-beta1-3 and TGF-betaI and betaII receptors in human peritoneal fibroblasts (HPF). TGF-beta isoforms and their receptors have been implicated as mediators of the healing process and adhesion development.

Methods: HPF were cultured under normal and hypoxic condition, and treated with and without (1 ng/mL) TGF-beta1 for 24 hr. Total RNA from each group was subjected to multiplex reverse transcriptase-polymerase chain reaction (RT/PCR) to quantitate TGF-beta1-3 and TGF-betaI and betaII receptors messenger RNA (mRNA) levels.

Results: Hypoxia resulted in a significant increase in TGF-beta1 (26%; P < 0.05), TGF-betaIR (34%; P < 0.05) and TGF-betaIIR (29%; P < 0.05) mRNA levels, with no effect on TGF-beta2 or beta3. TGF-beta1 treatment resulted in a significant increase in TGF-beta1 (35%; P < 0.05), but a decrease in TGF-beta2 (22%; P < 0.05) and no effect on TGF-beta3, TGF-betaIR or TGF-betaIIR. Combined treatment of hypoxia and TGF-beta1 caused a significant increase in TGF-beta1 (37%; P < 0.05), TGF-beta2 (12%; P < 0.05), TGF-betaIR (32%; P < 0.05) and TGF-betaIIR (34%; P < 0.05). There is no significant change in the mRNA levels of TGF-beta3 in any of the treatments.

Conclusion: Hypoxia and TGF-beta1 treatments of cultured HPF modulate the expression of TGF-beta1, beta2 and beta3 and their receptors betaIR and betaIIR by increasing the ratio of TGF-beta1 and beta2 to beta3, thus favoring the development of peritoneal adhesion.

Publication types

  • Comparative Study

MeSH terms

  • Activin Receptors, Type I / biosynthesis*
  • Activin Receptors, Type I / genetics
  • Cell Hypoxia / genetics*
  • Cells, Cultured / drug effects
  • Cells, Cultured / metabolism
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism*
  • Gene Expression Regulation* / drug effects
  • Humans
  • Peritoneal Diseases / etiology*
  • Peritoneum / cytology*
  • Protein Serine-Threonine Kinases
  • RNA, Messenger / biosynthesis
  • Receptor, Transforming Growth Factor-beta Type I
  • Receptor, Transforming Growth Factor-beta Type II
  • Receptors, Transforming Growth Factor beta / biosynthesis*
  • Receptors, Transforming Growth Factor beta / genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tissue Adhesions / etiology
  • Transforming Growth Factor beta / biosynthesis*
  • Transforming Growth Factor beta / genetics
  • Transforming Growth Factor beta / pharmacology
  • Transforming Growth Factor beta1
  • Transforming Growth Factor beta2
  • Transforming Growth Factor beta3
  • Wound Healing

Substances

  • RNA, Messenger
  • Receptors, Transforming Growth Factor beta
  • TGFB1 protein, human
  • TGFB2 protein, human
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1
  • Transforming Growth Factor beta2
  • Transforming Growth Factor beta3
  • Protein Serine-Threonine Kinases
  • Activin Receptors, Type I
  • Receptor, Transforming Growth Factor-beta Type I
  • Receptor, Transforming Growth Factor-beta Type II