A high concentration of collagen induces PLCγ2-independent aggregation.

PLCγ2-deficient (PLCγ2^−/−) and wild-type (WT) platelets were stimulated with a high level (50 μg/mL) of collagen. PLCγ2-deficient platelets aggregated in response to a high level of collagen, but the extent of aggregation was diminished in comparison to wild-type platelets (A). Aggregation of PLCγ2-deficient platelets preincubated with inhibitors (apyrase [10 U/mL], A3P5P [2 mM], AR-C69931MX [2 μM], and indomethacin [25μM]) and stimulated with 50 μg/mL collagen was inhibited by 10μg/mL hamster antimouse α_IIbβ₃ monoclonal antibody 1B5, but not by 10μg/mL hamster control IgG (B). PLCγ2-deficient platelets with and without inhibitors (apyrase [10 U/mL], A3P5P [2 mM], AR-C69931MX [2 μM], and indomethacin [25μM]) aggregated in response to a high level of collagen; the extents of aggregation were similar (C). PLCγ2-deficient platelets in the absence of inhibitors and wild-type platelets plus inhibitors (apyrase [10 U/mL], A3P5P [2 mM], AR-C69931MX [2 μM], and indomethacin [25μM]) aggregated to similar extents in response to a high level of collagen (D). Wild-type platelets treated with 4 inhibitors and PLCγ2-deficient platelets with and without inhibitors did not secrete TxA2 (E) even in response to a high concentration of collagen. Data were obtained from 6 tests. Bars represent means ± SEM.