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Celecoxib suppresses fibroblast proliferation and collagen expression by inhibiting ERK1/2 and SMAD2/3

Fengfeng Li1, Cunyi Fan, Bingfang Zeng

  • 1Department of Orthopaedics, The Sixth Affiliated People's Hospital, Shanghai Jiaotong University, Shanghai 200233, PR China.

Molecular Medicine Reports
|December 28, 2011
PubMed

Insights

Celecoxib inhibits fibroblast proliferation and collagen production by blocking key signaling pathways. This study demonstrates celecoxib

Area of Science:

  • Cell Biology
  • Pharmacology

Background:

  • Fibroblast proliferation and collagen expression are critical in wound healing and fibrosis.
  • Extracellular signal-regulated kinase 1/2 (ERK1/2) and SMAD2/3 pathways regulate these processes.
  • Understanding how drugs modulate these pathways is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the effects of celecoxib on fibroblast proliferation and collagen expression.
  • To determine if celecoxib inhibits these processes by modulating ERK1/2 and SMAD2/3 phosphorylation.

Main Methods:

  • NIH/3T3 fibroblasts were stimulated with fibroblast growth factor-2 (FGF-2) or transforming growth factor-β1 (TGF‑β1).
  • Celecoxib's effects on cell proliferation, viability, and apoptosis were assessed using MTT assays.
  • Quantitative RT-PCR and Western blot analysis were used to measure ERK1/2 and SMAD2/3 expression and phosphorylation.

Main Results:

  • Celecoxib suppressed FGF-2-stimulated fibroblast proliferation and viability.
  • Celecoxib induced apoptosis in NIH/3T3 fibroblasts.
  • Celecoxib inhibited TGF‑β1-stimulated collagen expression by reducing SMAD2/3 phosphorylation.
  • Celecoxib inhibited ERK1/2 phosphorylation, impacting fibroblast proliferation.

Conclusions:

  • Celecoxib effectively suppresses fibroblast proliferation and collagen expression.
  • The mechanism involves the inhibition of ERK1/2 and SMAD2/3 phosphorylation.
  • These findings suggest potential therapeutic applications for celecoxib in conditions involving excessive fibroblast activity.
Keywords:
fibrosiscelecoxibextracellular signal-regulated kinase MAP kinasesSMAD proteins

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