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  3. Peroxisome Proliferator-activated Receptor-γ Agonists Prevent In Vivo Remodeling Of Human Artery Induced By Alloreactive T Cells.
  1. Home
  3. Peroxisome Proliferator-activated Receptor-γ Agonists Prevent In Vivo Remodeling Of Human Artery Induced By Alloreactive T Cells.

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Peroxisome proliferator-activated receptor-γ agonists prevent in vivo remodeling of human artery induced by

Zuzana Tobiasova1, Lufeng Zhang, Tai Yi

  • 1Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.

Circulation
|June 22, 2011

View abstract on PubMed

Summary
This summary is machine-generated.

Peroxisome proliferator-activated receptor-gamma (PPARγ) agonists show promise in preventing vascular graft rejection by inhibiting human T cell responses. These findings suggest a potential new treatment for transplant rejection.

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Area of Science:

  • Immunology
  • Transplantation Biology
  • Pharmacology

Background:

  • Peroxisome proliferator-activated receptor-gamma (PPARγ) ligands possess anti-inflammatory properties.
  • Allogeneic T cell responses drive vascular graft rejection, leading to graft loss.
  • Rodent studies suggest PPARγ agonists may prevent vascular rejection, but human responses remain unclear.

Purpose of the Study:

  • To investigate the effects of PPARγ agonists on human vascular graft rejection.
  • To determine the role of PPARγ in human T cell responses to allogeneic vascular cells.

Main Methods:

  • A human vascular graft rejection model in immunodeficient mice using human artery and allogeneic human peripheral blood mononuclear cells.
  • Administration of PPARγ agonists (15-deoxy-prostaglandin-J(2), ciglitazone, pioglitazone) and a PPARγ antagonist (GW9662).
  • Assessment of intimal thickening, T cell infiltration, inflammatory cytokine levels, and in vitro T cell proliferation and migration.

    • Main Results:

    • PPARγ agonists significantly reduced intimal expansion, T cell infiltration, and inflammatory cytokine levels.
    • The PPARγ antagonist GW9662 reversed the protective effects of PPARγ agonists.
    • In vitro, pioglitazone inhibited alloantigen-induced T cell proliferation and transendothelial migration.

    Conclusions:

    • PPARγ agonists effectively inhibit allogeneic human memory T cell responses in a vascular graft rejection model.
    • PPARγ agonists represent a potential therapeutic strategy for treating vascular graft rejection.