PPARβ/δ Agonists Modulate Platelet Function via a Mechanism Involving PPAR Receptors and Specific Association/Repression of PKCα

PPARβ/δ Agonists Modulate Platelet Function via a Mechanism Involving PPAR Receptors and Specific Association/Repression of PKCα–Brief Report

Published:2009-11 Issue:11 Volume:29 Page:1871-1873
ISSN:1079-5642
Container-title:Arteriosclerosis, Thrombosis, and Vascular Biology
language:en
Short-container-title:ATVB

Author:

Ali Ferhana Y.¹,Hall Matthew G.¹,Desvergne Béatrice¹,Warner Timothy D.¹,Mitchell Jane A.¹

Affiliation:

1. From Cardiothoracic Pharmacology (F.Y.A., J.A.M.), National Heart and Lung Institute, Imperial College London, UK; Queen Mary University of London (F.Y.A., T.D.W.), Barts and the London School of Medicine and Dentistry, The William Harvey Research Institute, UK and the Center for Integrative Genomics (M.G.H., B.D.), University of Lausanne, Switzerland.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

Reference8 articles.

1. Role of nuclear receptor signaling in platelets: antithrombotic effects of PPARβ

2. Role of Prostacyclin versus Peroxisome Proliferator-Activated Receptor β Receptors in Prostacyclin Sensing by Lung Fibroblasts

3. Direct Demonstration of Involvement of Protein Kinase Cα in the Ca2+-induced Platelet Aggregation

4. Identification of Protein Kinase Cα as an Essential, but Not Sufficient, Cytosolic Factor for Ca2+-induced α- and Dense-core Granule Secretion in Platelets

5. PPARγ1 attenuates cytosol to membrane translocation of PKCα to desensitize monocytes/macrophages

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