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. 2019 Jul 4;105(4):1095–1106. doi: 10.3324/haematol.2018.214460

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Figure 3. — Dynamics of cytoplasmic calcium, mitochondrial potentials and phosphatidylserine exposure of single platelets. Plots show dynamics of intracellular calcium concentration and annex-in V binding to single platelets during incubation on fibrinogen in the presence of 1.5 mM of extracellular calcium. (A) Averaged calcium dynamics (± standard deviation) for non-activated (N/A) platelets from patients with Wiskott-Aldrich syndrome (WAS) (4 patients, 34 platelets) and for platelets from healthy donors (HD) which were either activated with 10 μM TRAP (3 HD, 30 platelets) or not activated (3 HD, 26 platelets). (B) Dynamics for a single healthy phosphatidylserine-negative (PS⁻) platelet; (C) the same for a WAS PS⁻ platelet; (D) the same for a WAS PS⁺ platelet. The TMRM signal is represented as a number of TMRM-positive mitochondria in the platelet (B-D). Intracellular events leading to PS exposure induced with mitochondria collapse with following cytoplasmic calcium increase and PS exposure. All three processes were almost simultaneous, lasting decades of seconds. Both WAS (E) and normal (not shown) PS⁺ platelets lost their mitochondrial potentials. Scale bar: 1 μm for all microscopic images. TRAP: thrombin receptor agonist peptide; TMRM: tetramethylrhodamine methyl ester.