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Updated: Jun 26, 2026
Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
Published on: July 28, 2023
Troglitazone suppresses transforming growth factor-beta1-induced collagen type I expression in keloid fibroblasts
1Department of Hand and Plastic Surgery, Second Affiliated Hospital of Wenzhou Medical College, Xueyuan West Road 109, Wenzhou 325027, Zhejiang Province, China. guoyou.zhang@yahoo.com
Background:
Peroxisome proliferator-activated receptor (PPAR)-gamma agonists are increasingly used in patients with diabetes and some studies have suggested a beneficial effect on organ fibrosis. However their effects on dermal fibrosis in keloids are unknown.
Objective:
To investigate the effect of the PPAR-gamma agonist troglitazone on transforming growth factor (TGF)-beta1-induced collagen type I expression in keloid fibroblasts.
Methods:
Keloid fibroblasts were cultured and exposed to different concentrations of troglitazone in the presence of TGF-beta1. The mRNA expression of PPAR-gamma was determined by semiquantitative reverse transcriptase-polymerase chain reaction. The protein of PPAR-gamma, Smad2, Smad3, phoshpo-Smad2/3 and collagen type I was determined by Western blotting and collagen synthesis was evaluated by measuring (3)H-proline incorporation. The effect of troglitazone on cell viability was evaluated by the colorimetric conversion of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide.
Results:
PPAR-gamma was expressed at a moderate level in keloid fibroblasts. Troglitazone depressed TGF-beta1-stimulated collagen type I expression and collagen synthesis in keloid fibroblasts in a concentration-dependent manner. Moreover, troglitazone inhibited expression and phosphorylation of TGF-beta1-induced Smad2/3. Cell viability was unaffected. These inhibitory effects of troglitazone were reversed by the PPAR-gamma-specific antagonist GW9662.
Conclusions:
Our data suggest that PPAR-gamma is present in keloid fibroblasts and PPAR-gamma activation inhibits TGF-beta1-induced collagen type I expression at least in part by decreasing collagen synthesis. PPAR-gamma may be a promising therapeutic target for keloids.
Insights
Peroxisome proliferator-activated receptor (PPAR)-gamma agonists, like troglitazone, reduce collagen production in keloid fibroblasts. This suggests PPAR-gamma activation is a potential therapeutic target for keloid scar treatment.
Area of Science:
- Dermatology
- Fibrosis Research
- Molecular Biology
Background:
- Peroxisome proliferator-activated receptor (PPAR)-gamma agonists show promise in treating organ fibrosis.
- Their efficacy in addressing dermal fibrosis, specifically in keloids, remains unexplored.
Purpose of the Study:
- To investigate the impact of the PPAR-gamma agonist troglitazone on transforming growth factor (TGF)-beta1-induced collagen type I expression in keloid fibroblasts.
Main Methods:
- Keloid fibroblasts were treated with troglitazone and TGF-beta1.
- Collagen type I expression, synthesis, and related signaling pathways (Smad2/3) were analyzed.
- PPAR-gamma expression and antagonist effects were assessed.
Main Results:
- Troglitazone significantly reduced TGF-beta1-stimulated collagen type I expression and synthesis in keloid fibroblasts.
- Inhibition of collagen production was concentration-dependent and mediated via Smad2/3 signaling.
- The effects were reversed by a PPAR-gamma antagonist, confirming the pathway.
Conclusions:
- PPAR-gamma is present in keloid fibroblasts and its activation inhibits collagen type I expression.
- PPAR-gamma activation reduces collagen synthesis, indicating its potential as a therapeutic target for keloids.
