Figure 2
Figure 2. Increased IAC-1 binding to α2β1 on RGDS-treated washed platelets and involvement of tyrosine kinases and actin in this signaling. (A) Flow cytometric experiments detecting IAC-1, collagen, and anti–P-selectin binding to resting washed platelets (□), to RGDS-treated washed platelets (⊡), and to CVX-stimulated washed platelets in the presence of 100μg/mL fibrinogen (▪) or to aggrastat-treated washed platelets (▨). (B) Flow cytometric experiments of IAC-1 binding to RGDS- and CVX-stimulated platelets in the absence (□) or presence (⊡) of PGE1 (5 μM). (C) Flow cytometric experiments of IAC-1 binding to RGDS-triggered platelets incubated with 5 μM PGE1 in the absence (□) or presence (⊡) of staurosporin (2 μM), Ro 31-8220 (10 μM), genistein (50 μg/mL), or PP2 (10 μM). All data are expressed as the mean ± SEM of at least 3 independent experiments.

Increased IAC-1 binding to α2β1 on RGDS-treated washed platelets and involvement of tyrosine kinases and actin in this signaling. (A) Flow cytometric experiments detecting IAC-1, collagen, and anti–P-selectin binding to resting washed platelets (□), to RGDS-treated washed platelets (⊡), and to CVX-stimulated washed platelets in the presence of 100μg/mL fibrinogen (▪) or to aggrastat-treated washed platelets (▨). (B) Flow cytometric experiments of IAC-1 binding to RGDS- and CVX-stimulated platelets in the absence (□) or presence (⊡) of PGE1 (5 μM). (C) Flow cytometric experiments of IAC-1 binding to RGDS-triggered platelets incubated with 5 μM PGE1 in the absence (□) or presence (⊡) of staurosporin (2 μM), Ro 31-8220 (10 μM), genistein (50 μg/mL), or PP2 (10 μM). All data are expressed as the mean ± SEM of at least 3 independent experiments.

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