Fig. 8

Type II PI3 kinase C2 α activity modulates \(\dot{\varepsilon}\)-S [Ca²⁺]_c flux. A Ca²⁺ sampling along T14 in θ = 80° stenosis geometry following treatment of reconstituted blood (10 min) with DMSO (0.1%v/v) [N = 8 experiments]; Copanlisib (10 μM) [N = 3 experiments]; Wortmannin (100 nM) [N = 3 experiments]; AS252424 (2 μM) [N = 3 experiments]; TGX221 (0.5 μM) [N = 3 experiments]; MIPS-21335 (10 μM) [N = 4 experiments]; CM-851-106A (10 μM) [N = 4 experiments]. B Frequency histogram showing the overall distribution of platelet [Ca²⁺]_c (10 nM bins) within Hyperbolic flow at Q = 600 μL/min: DMSO (0.1%v/v); MIPS-21335 (10 μM); CM-851-106A (10 μM). C Platelet aggregation at stenosis apex θ = 80° following treatment of DiOC₆ labelled human whole blood with, DMSO (0.1%v/v) [N = 6 experiments]; MIPS-21335 (10 μM) [N = 6 experiments]; MIPS-21335 (1 μM) [N = 3 experiments]; CM-851-106A (10 μM) [N = 4 experiments]. Curves shown are [Agonist] vs. response Variable slope (four parameters) least squares fit + 95% CI. D Ca²⁺ sampling along T14 in θ = 20° stenosis geometry following treatment of reconstituted blood (10 min) with DMSO (0.1%v/v) [N = 10 experiments]; Yoda1 (25 μM) [N = 9 experiments]; Yoda1 (25 μ M) + MIPS-21335 (10 μM) [N = 3 experiments]. E Ca²⁺ sampling along T14 in θ_e = 80° stenosis geometry following treatment of reconstituted blood (10 min) with DMSO (0.1%v/v) [N = 3 experiments]; Latrunculin B (8 μM) [N = 3 experiments]; Jasplakinolide (5 μM) [N = 3 experiments]; Blebbistatin (10 μM) [N = 3 experiments]; Cytochalasin D (5 μM) [N = 3 experiments]