Rosiglitazone alleviates the persistent fibrotic phenotype of lesional skin scleroderma fibroblasts

Rheumatology (Oxford). 2010 Feb;49(2):259-63. doi: 10.1093/rheumatology/kep371. Epub 2009 Dec 9.


Objective: The transcription factor peroxisome proliferator-activated receptor (PPAR)-gamma plays an important role in controlling cell differentiation. The aim of the present study was to examine whether PPAR-gamma expression was reduced in skin scleroderma fibroblasts and whether PPAR-gamma agonists could suppress the persistent fibrotic phenotype of skin scleroderma fibroblasts.

Methods: Dermal fibroblasts were isolated from site-, age- and sex-matched healthy individuals and lesional areas of individuals with dcSSc. Western blot and collagen gel contraction analyses were used to detect protein expression in the presence or absence of the PPAR-gamma agonist rosiglitazone.

Results: PPAR-gamma expression was reduced in dcSSc fibroblasts. The PPAR-gamma agonist rosiglitazone alleviated the persistent fibrotic phenotype of dcSSc fibroblasts.

Conclusion: Rosiglitazone may alleviate the extent of fibrosis in dcSSc.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Adult
  • Cells, Cultured
  • Female
  • Fibroblasts / drug effects*
  • Fibroblasts / metabolism
  • Fibrosis
  • Humans
  • Male
  • Middle Aged
  • PPAR gamma / agonists
  • PPAR gamma / metabolism
  • Phenotype
  • Rosiglitazone
  • Scleroderma, Localized / metabolism
  • Scleroderma, Localized / pathology*
  • Skin / metabolism
  • Skin / pathology*
  • Thiazolidinediones / pharmacology*


  • ACTA2 protein, human
  • Actins
  • PPAR gamma
  • Thiazolidinediones
  • Rosiglitazone