Arterioscler Thromb Vasc Biol PPARβ/δ Agonists Modulate Platelet Function via a Mechanism Involving PPAR Receptors and Specific Association/Repression of PKCα–Brief Report by Ferhana Y. Ali, Matthew G. Hall, Béatrice Desvergne, Timothy D. Warner, and Jane A. Mitchell Arterioscler Thromb Vasc Biol Volume 29(11):1871-1873 November 1, 2009 Copyright © American Heart Association, Inc. All rights reserved.

Figure 1. A, Western blot of PKCα in PRP incubated with GW501516 (GW; 1 μmol/L, 3 μmol/L, 10 μmol/L) using samples that were either immunoprecipitated with PPARβ/δ beforehand (homogenate IP) or not (total homogenate). Figure 1. A, Western blot of PKCα in PRP incubated with GW501516 (GW; 1 μmol/L, 3 μmol/L, 10 μmol/L) using samples that were either immunoprecipitated with PPARβ/δ beforehand (homogenate IP) or not (total homogenate). B, Densitometry for the imunoprecipitation results only. C, PKCα activation after incubation with GW501516 (1 μmol/L) for an increasing amount of time. Vehicle sample (V) was taken after 30 minutes incubation. Blots shown are representative of 3 to 4 experiments. *P<0.05 for vehicle vs treated; 1-way ANOVA followed by Dunnett post test. Ferhana Y. Ali et al. Arterioscler Thromb Vasc Biol. 2009;29:1871-1873 Copyright © American Heart Association, Inc. All rights reserved.

Figure 2. A, Effect of GW501516 (GW) in murine PRP on (A) cAMP release, (B) ADP-induced adhesion, and (C) ADP-induced aggregation. Figure 2. A, Effect of GW501516 (GW) in murine PRP on (A) cAMP release, (B) ADP-induced adhesion, and (C) ADP-induced aggregation. Data in B and C are represented as % compared to ADP control for each genotype. n=3 experiments, each using PRP pooled from 8 to 12 mice. *P<0.05 for differences between control and treated group; 1-way ANOVA (A) or t test (B and C). #P<0.05 for differences between WT and PPARβ/δ−/− within treatment group; 2-way ANOVA. Ferhana Y. Ali et al. Arterioscler Thromb Vasc Biol. 2009;29:1871-1873 Copyright © American Heart Association, Inc. All rights reserved.