Figure 7.

Palmitoylated peptide pR724-R734 (pRKEFAKFEEER) inhibited low-level γ-thrombin–induced αIIbβ3-mediated outside-in signaling and its associated TxA₂ production and ATP secretion. (A) Aggregation traces of normal platelets treated with low-level γ-thrombin (5 nM) in the presence of 7E3 (10 μg/mL), the palmitoylated peptide p-R724-R734 (pRKEFAKFEEER, 10 μM) with or without Fg (250 μg/mL), a scrambled, palmitoylated control peptide (pEAERKFERKFE, 10 μM), a nonpalmitoylated version of peptide R724-R734, (RKEFAKFEEER, 10 μM), or the palmitoylated peptide pA735-N744 (pARAKWDTANN, 10 μM). In contrast to pARAKWDTANN and the control peptides, 7E3 and pRKEFAKFEEER inhibited aggregation induced by low-level γ-thrombin. Exogenous Fg restored aggregation to platelets treated with pRKEFAKFEEER. (B) TxA₂ production (left) and ATP secretion (right) by normal platelets treated with γ-thrombin alone or in the presence of 7E3 (10 μg/mL), pRKEFAKFEEER (10 μM) with or without Fg, or the control peptides (10 μM). There are no significant differences (P < .05) between the values of 7E3 and pRKEFAKFEEER with or without Fg-treated platelets for TxA₂ production and ATP secretion. The error bars represent SD, n = 3.