Fig. 3.
Fig. 3. A high concentration of collagen can induce secretion-independent aggregation. / Tp-deficient platelets were stimulated with a high concentration (50 μg/mL) of collagen in the presence of 10 μM Ro31-8220 (a PKC inhibitor that prevents secretion) or dimethyl sulfoxide (DMSO) as a control. Ro31-8220 did not prevent aggregation induced by a high level of collagen but did affect the maximal aggregation response (A). Collagen (50 μg/mL)–induced aggregation of Ro31-8220–treated Tp-deficient platelets was inhibited by incubating the platelets with 10μg/mL hamster monoclonal antimouse αIIbβ3 antibody 1B5, but not by 10μg/mL hamster control IgG (B). Treatment of Tp-deficient platelets with Ro31-8220 prevents collagen-induced ATP secretion (C) but does not affect TxA2 production (D). Thus, Ro31-8220 affects only PKC activation and secretion and does not affect collagen-induced TxA2 production. Data were obtained from 3 tests. Bars represent means ± SEM.

A high concentration of collagen can induce secretion-independent aggregation.

Tp-deficient platelets were stimulated with a high concentration (50 μg/mL) of collagen in the presence of 10 μM Ro31-8220 (a PKC inhibitor that prevents secretion) or dimethyl sulfoxide (DMSO) as a control. Ro31-8220 did not prevent aggregation induced by a high level of collagen but did affect the maximal aggregation response (A). Collagen (50 μg/mL)–induced aggregation of Ro31-8220–treated Tp-deficient platelets was inhibited by incubating the platelets with 10μg/mL hamster monoclonal antimouse αIIbβ3 antibody 1B5, but not by 10μg/mL hamster control IgG (B). Treatment of Tp-deficient platelets with Ro31-8220 prevents collagen-induced ATP secretion (C) but does not affect TxA2 production (D). Thus, Ro31-8220 affects only PKC activation and secretion and does not affect collagen-induced TxA2 production. Data were obtained from 3 tests. Bars represent means ± SEM.

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