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Effect of celecoxib on proliferation, collagen expression, ERK1/2 and SMAD2/3 phosphorylation in NIH/3T3 fibroblasts

Fengfeng Li1, Shen Liu, Yuanming Ouyang

  • 1Department of Orthopaedics, The Sixth Affiliated People's Hospital, Shanghai Jiaotong University School of Medicine, 600 Yishan Road, Shanghai 200233, China.

European Journal of Pharmacology
|January 3, 2012
PubMed

Insights

Celecoxib inhibits fibroblast proliferation and collagen production by blocking ERK1/2 and SMAD2/3 phosphorylation. This study investigates celecoxib

Area of Science:

  • Pharmacology
  • Cell Biology
  • Biochemistry

Background:

  • Fibroblast proliferation and collagen synthesis are critical in tissue repair and fibrosis.
  • Understanding the molecular mechanisms regulating these processes is essential for developing targeted therapies.

Purpose of the Study:

  • To investigate the effects of celecoxib on NIH/3T3 fibroblast proliferation and collagen expression.
  • To elucidate the impact of celecoxib on ERK1/2 and SMAD2/3 signaling pathways.

Main Methods:

  • NIH/3T3 fibroblasts were stimulated with fibroblast growth factor-2 (FGF-2) or transforming growth factor-β1 (TGF-β1) in the presence of celecoxib.
  • Cell proliferation was assessed using MTT assays.
  • Gene and protein expression, as well as phosphorylation levels of ERK1/2 and SMAD2/3, were analyzed via quantitative RT-PCR and Western blotting.

Main Results:

  • Celecoxib suppressed FGF-2 and TGF-β1-stimulated fibroblast proliferation with IC50 values of 75±1.9μmol/l and 48±1.4μmol/l, respectively.
  • Celecoxib inhibited ERK1/2 phosphorylation but not ERK1/2 expression.
  • Celecoxib reduced collagen type I and III expression by inhibiting SMAD2/3 phosphorylation without affecting SMAD2/3 expression.

Conclusions:

  • Celecoxib effectively suppresses fibroblast proliferation and collagen production.
  • The mechanism involves the inhibition of ERK1/2 and SMAD2/3 phosphorylation pathways.
  • These findings suggest celecoxib's potential therapeutic role in conditions characterized by excessive fibroblast activity.

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