Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Br J Dermatol. 2013 Jan;168(1):129-35. doi: 10.1111/j.1365-2133.2012.11199.x. Epub 2012 Oct 5.

Peroxisome proliferator-activated receptor γ agonists reduce cell proliferation and viability and increase apoptosis in systemic sclerosis fibroblasts.

Author information

  • 1Department of Internal Medicine, Metabolism Unit, University of Pisa School of Medicine, Via Roma 67, I-56100 Pisa, Italy. alessandro.antonelli@med.unipi.it

Abstract

BACKGROUND:

 No study has evaluated the effect of the peroxisome proliferator-activated receptor γ (PPARγ) agonists on cell viability, proliferation and apoptosis in cultured systemic sclerosis (SSc) fibroblasts.

OBJECTIVES:

The effects of two pure PPARγ agonists (rosiglitazone and pioglitazone) in cultured SSc fibroblasts were evaluated and compared with effects in normal fibroblasts.

METHODS:

 The study included evaluation of cell viability and proliferation (based on the cleavage of tetrazolium salts and measurement of absorbance of the cell proliferation reagent WST-1), and determination of cell apoptosis (by means of the Hoechst dye uptake).

RESULTS:

Rosiglitazone or pioglitazone (20μmolL(-1) ) significantly reduced cell proliferation (cell count of 75% and 83% compared with baseline, respectively, after 2h) and cell viability (absorbance reductions of 25% and 22% compared with baseline, respectively, after 2 h), and increased apoptosis (apoptotic cell percentages 9·9% and 8·6%, respectively, after 48h of incubation) in SSc fibroblasts, whereas they did not present a significant influence on control fibroblasts.

CONCLUSIONS:

The effects of rosiglitazone or pioglitazone shown on SSc fibroblasts raise the hypothesis of a therapeutic role for PPARγ agonists in patients affected by SSc.

© 2012 The Authors. BJD © 2012 British Association of Dermatologists.

PMID:
22860752
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Blackwell Publishing
    Loading ...
    Write to the Help Desk