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Rosiglitazone alleviates the persistent fibrotic phenotype of lesional skin scleroderma fibroblasts
Xu Shi-wen1, Mark Eastwood, Richard J Stratton
1Centre for Rheumatology, University College London (Royal Free Campus), London, UK.
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.
Insights
Peroxisome proliferator-activated receptor (PPAR)-gamma is reduced in diffuse cutaneous systemic sclerosis (dcSSc) fibroblasts. PPAR-gamma agonists like rosiglitazone may help reduce fibrosis in dcSSc.
Area of Science:
- Dermatology
- Molecular Biology
- Fibrosis Research
Background:
- Peroxisome proliferator-activated receptor (PPAR)-gamma is a key regulator of cell differentiation.
- Fibrosis is a hallmark of systemic sclerosis, a condition characterized by excessive connective tissue deposition.
Purpose of the Study:
- To investigate PPAR-gamma expression levels in skin scleroderma fibroblasts.
- To determine if PPAR-gamma agonists can mitigate the fibrotic phenotype of these cells.
Main Methods:
- Dermal fibroblasts were isolated from healthy individuals and patients with diffuse cutaneous systemic sclerosis (dcSSc).
- Western blot and collagen gel contraction assays were performed.
- The effect of the PPAR-gamma agonist rosiglitazone was evaluated.
Main Results:
- PPAR-gamma expression was found to be decreased in dcSSc fibroblasts compared to healthy controls.
- Treatment with rosiglitazone effectively reduced the fibrotic characteristics of dcSSc fibroblasts.
- Rosiglitazone alleviated the persistent fibrotic phenotype observed in dcSSc fibroblasts.
Conclusions:
- Reduced PPAR-gamma expression is implicated in the pathogenesis of dcSSc.
- PPAR-gamma agonists, such as rosiglitazone, show potential as a therapeutic strategy to manage fibrosis in dcSSc.
