Expression of matrix metalloproteinases in cyclosporin-treated gingival fibroblasts is regulated by transforming growth factor (TGF)-beta1 autocrine stimulation

J Periodontol. 2002 Nov;73(11):1313-22. doi: 10.1902/jop.2002.73.11.1313.

Abstract

Background: Gingival overgrowth is a common side effect following the administration of cyclosporin A (CsA). The pathogenesis of this condition is not fully understood; however, recent studies show that CsA regulates the transcription of several cytokines including transforming growth factor-beta1 (TGF-beta1). The aim of this study was to investigate the potential role of TGF-beta1 in the pathogenesis of CsA-induced gingival overgrowth, exploring a possible autocrine stimulation of TGF-beta1 as a cellular regulator of synthesis of matrix metalloproteinases (MMPs) and its tissue inhibitors (TIMPs).

Methods: Gingival fibroblasts from human normal gingiva were incubated with increasing concentrations of CsA, cultured for 24 hours, and the expression and production of TGF-beta1 determined by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. MMP and TIMP mRNA expression levels were also analyzed by RT-PCR. To determine the effect of TGF-beta1 on the expression of MMP and TIMP by human gingival fibroblasts under CsA treatment, human gingival fibroblast cultures were treated with sense oligonucleotides (SON) or antisense oligonucleotides (AON).

Results: CsA simultaneously stimulated TGF-beta1 expression and production and inhibited expression of MMP-1 and MMP-2 by human gingival fibroblasts, whereas CsA has a slight effect on TIMP-1 and TIMP-2 expression. AON reduced TGF-beta1 production as demonstrated by ELISA, whereas TGF-beta1 mRNA expression levels were not significantly modified. The inhibition of TGF-beta1 production by AON modulated MMP expression, demonstrating the autocrine inhibitory effect of TGF-beta1 in CsA-treated human gingival fibroblasts.

Conclusions: The data presented here suggest that TGF-beta1 in an autocrine fashion may contribute to a reduction of proteolytic activity of human gingival fibroblasts in CsA-induced gingival overgrowth, which favors the accumulation of extracellular matrix.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Cells, Cultured
  • Cyclosporine / pharmacology*
  • Down-Regulation
  • Enzyme Inhibitors / pharmacology*
  • Enzyme-Linked Immunosorbent Assay
  • Fibroblasts / drug effects
  • Fibroblasts / enzymology
  • Gingiva / cytology
  • Gingiva / drug effects*
  • Gingiva / enzymology
  • Gingival Overgrowth / chemically induced*
  • Gingival Overgrowth / enzymology*
  • Humans
  • Matrix Metalloproteinase Inhibitors
  • Matrix Metalloproteinases / biosynthesis*
  • Oligonucleotides, Antisense / pharmacology
  • Peptide Chain Initiation, Translational / drug effects
  • RNA, Messenger / analysis
  • RNA, Messenger / biosynthesis
  • Reverse Transcriptase Polymerase Chain Reaction
  • Statistics, Nonparametric
  • Tissue Inhibitor of Metalloproteinases / biosynthesis
  • Transforming Growth Factor beta / biosynthesis
  • Transforming Growth Factor beta / drug effects
  • Transforming Growth Factor beta / physiology*
  • Transforming Growth Factor beta1

Substances

  • Enzyme Inhibitors
  • Matrix Metalloproteinase Inhibitors
  • Oligonucleotides, Antisense
  • RNA, Messenger
  • TGFB1 protein, human
  • Tissue Inhibitor of Metalloproteinases
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1
  • Cyclosporine
  • Matrix Metalloproteinases