Figure 5.
Figure 5. Platelet ATP secretion in response to agonist stimulation. Secretion of washed platelets was measured at 37°C by the turbidometric method in a Lumi-dual Aggregometer following the addition of various agonists. Secretion induced by low doses of ADP or U46619 (thromboxane A2 analog) was impaired in PLCβ2/β3 knock-out platelets (A). Shown are means ± standard error of 3 experiments. Similar results were seen in 7 experiments analyzing secretion in platelet-rich plasma. (B) A graph showing an analysis of the agonist-induced secretion response of PI3Kγ-null platelets compared with control cells. Paired student t testing revealed no significant defect in PI3Kγ knock-out platelets with any agonist. Shown are the means ± SEM normalized in 2 experiments. A similar lack of secretion defect was found in 3 experiments analyzing secretion in platelet-rich plasma (not shown).

Platelet ATP secretion in response to agonist stimulation. Secretion of washed platelets was measured at 37°C by the turbidometric method in a Lumi-dual Aggregometer following the addition of various agonists. Secretion induced by low doses of ADP or U46619 (thromboxane A2 analog) was impaired in PLCβ2/β3 knock-out platelets (A). Shown are means ± standard error of 3 experiments. Similar results were seen in 7 experiments analyzing secretion in platelet-rich plasma. (B) A graph showing an analysis of the agonist-induced secretion response of PI3Kγ-null platelets compared with control cells. Paired student t testing revealed no significant defect in PI3Kγ knock-out platelets with any agonist. Shown are the means ± SEM normalized in 2 experiments. A similar lack of secretion defect was found in 3 experiments analyzing secretion in platelet-rich plasma (not shown).

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