Figure 5.
Figure 5. PPARγ agonists block platelet release of CD40L and TXB2. Purified human platelets were exposed to buffer or with 20 μM 15d-PGJ2 or rosiglitazone for 15 minutes. The platelets were then activated with 0.8 U/mL thrombin and the supernatants collected at the times shown. Specific ELISA and enzyme immunoassays for CD40L (A) and TXB2 (B) levels were performed. (A) The increase in supernatant CD40L over time was statistically significant after thrombin activation compared with untreated or PPARγ agonist pretreated samples (P = .0006 by the log-rank test). There were no significant differences in CD40L release when comparing untreated samples with those treated with PPARγ agonist and thrombin. Mean ± SD values are shown. (B) The increase in supernatant TXB2 over time was statistically significant after thrombin activation compared with untreated or PPARγ agonist and thrombin-treated platelets (P = .0004 by the log-rank test). These data are representative of 3 separate experiments. *Significantly different from samples treated with 15d-PGJ2 or rosiglitazone.

PPARγ agonists block platelet release of CD40L and TXB2. Purified human platelets were exposed to buffer or with 20 μM 15d-PGJ2 or rosiglitazone for 15 minutes. The platelets were then activated with 0.8 U/mL thrombin and the supernatants collected at the times shown. Specific ELISA and enzyme immunoassays for CD40L (A) and TXB2 (B) levels were performed. (A) The increase in supernatant CD40L over time was statistically significant after thrombin activation compared with untreated or PPARγ agonist pretreated samples (P = .0006 by the log-rank test). There were no significant differences in CD40L release when comparing untreated samples with those treated with PPARγ agonist and thrombin. Mean ± SD values are shown. (B) The increase in supernatant TXB2 over time was statistically significant after thrombin activation compared with untreated or PPARγ agonist and thrombin-treated platelets (P = .0004 by the log-rank test). These data are representative of 3 separate experiments. *Significantly different from samples treated with 15d-PGJ2 or rosiglitazone.

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