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A Novel In Vitro Wound Healing Assay to Evaluate Cell Migration
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Published on: March 17, 2018

PPAR ligands decrease human airway smooth muscle cell migration and extracellular matrix synthesis.

Jancy Stephen1, Chris Delvecchio, Naomi Spitale

  • 1Firestone Institure for Respiratory Health, St Joseph's Healthcare, Dept of Medicine, McMaster University, Hamilton, Ontario, Canada.

The European Respiratory Journal
|June 2, 2012
PubMed
Summary
This summary is machine-generated.

Peroxisome proliferator-activated receptor (PPAR) ligands reduce airway smooth muscle cell migration and extracellular matrix production. These findings suggest PPAR ligands may be beneficial for managing airway remodeling.

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Area of Science:

  • Cell Biology
  • Pharmacology
  • Respiratory Medicine

Background:

  • Airway smooth muscle cells (HASM) produce extracellular matrix (ECM) proteins, influencing smooth muscle survival, proliferation, and migration.
  • Current therapies are largely ineffective against HASM matrix production and migration, key factors in airway remodeling.
  • Peroxisome proliferator-activated receptor (PPAR) ligands have shown potential in reducing migration and matrix production in other cell types.

Purpose of the Study:

  • To investigate the effects of PPAR ligands on matrix production and migration in human airway smooth muscle (HASM) cells.
  • To determine the expression and activity of PPARs in HASM cells.
  • To elucidate the mechanisms underlying the effects of PPAR ligands on HASM cells.

Main Methods:

  • RT-PCR and Western blotting were used to assess PPAR expression (PPARα, β, and γ) in HASM cells.
  • A PPAR response element-luciferase reporter plasmid was used to confirm endogenous PPAR activity.
  • HASM cells were treated with specific PPAR ligands (ciglitazone, 15-deoxy-Δ12,14-prostaglandin J(2), WY-14643) to evaluate effects on migration and ECM (collagen, fibronectin) secretion.

Main Results:

  • HASM cells express PPARα, β, and γ, with demonstrated endogenous PPAR activity.
  • PPAR ligands significantly reduced HASM cell migration induced by platelet-derived growth factor.
  • Ligands also inhibited collagen and fibronectin secretion, partly via cyclooxygenase-2 induction and prostaglandin E(2) production, leading to increased cyclic AMP levels.

Conclusions:

  • PPAR ligands effectively decrease migration and matrix production in HASM cells.
  • The observed effects are not mediated by inhibiting Akt phosphorylation or promoting PTEN activity.
  • PPAR ligands represent a potential therapeutic strategy for modulating airway remodeling.