Figure 4
Figure 4. [Ca2+]i elevations in platelets interacting with an immobilized anti-integrin β1 monoclonal antibody or with the α2β1-specific triple-helical GFOGER peptide. Blood cell suspensions (Figure 1 legend contains details) were perfused at the shear rate of 250 seconds over the anti-β1 antibody TS2/16 (A-B) or the peptide GFOGER (C). (A) Typical α-like (short-lasting) [Ca2+]i peaks were identified in platelets interacting with TS2/16. (B) Blood cell suspensions were perfused over TS2/16 without or with prior treatment for 10 minutes at 37°C with the anti-GPVI monoclonal antibody Fab 9O12.2 (50 μg/mL) or the Src kinase inhibitor PP2 at the indicated concentrations. Results are expressed as described in the legend to Figure 2 (n = 3); note the absence of γ-like peaks under these conditions. (C) Typical α-like peaks were seen in platelets (5 × 107/mL) interacting with the GFOGER peptide (coating solution concentration: 50 μg/mL).

[Ca2+]i elevations in platelets interacting with an immobilized anti-integrin β1 monoclonal antibody or with the α2β1-specific triple-helical GFOGER peptide. Blood cell suspensions (Figure 1 legend contains details) were perfused at the shear rate of 250 seconds over the anti-β1 antibody TS2/16 (A-B) or the peptide GFOGER (C). (A) Typical α-like (short-lasting) [Ca2+]i peaks were identified in platelets interacting with TS2/16. (B) Blood cell suspensions were perfused over TS2/16 without or with prior treatment for 10 minutes at 37°C with the anti-GPVI monoclonal antibody Fab 9O12.2 (50 μg/mL) or the Src kinase inhibitor PP2 at the indicated concentrations. Results are expressed as described in the legend to Figure 2 (n = 3); note the absence of γ-like peaks under these conditions. (C) Typical α-like peaks were seen in platelets (5 × 107/mL) interacting with the GFOGER peptide (coating solution concentration: 50 μg/mL).

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