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. 2022 Dec 21;18(11):3067–3073. doi: 10.1111/jth.15107

FIGURE 1.

FIGURE 1

Altered mitochondrial function reduces procoagulant platelet formation. Platelets were isolated from healthy donors and COVID‐19 patients. A, Phosphatidylserine (PS) exposure was assessed by flow cytometry using annexin V binding under resting conditions and after dual agonist stimulation (1 U/mL thrombin + 250 ng/mL convulxin). Representative flow plots are shown. B, The percentage of platelets with high PS exposure was quantified (n = 11). Open circles represent non–intensive care unit (ICU) patients, closed circles represent ICU patients. C, Platelet PS exposure in response to 50 µmol/L A23187 was measured by annexin V binding. Representative flow plots are shown. D, Mean fluorescence intensity (MFI) of annexin V staining after A23187 treatment (n = 3‐4). E, Platelet mitochondrial membrane potential was measured by tetramethylrhodamine methyl ester staining analyzed by flow cytometry under resting conditions and after dual agonist stimulation (1 U/mL thrombin + 250 ng/mL convulxin; n = 5). F, Mitochondrial reactive oxygen species was measured by MitoSOX staining analyzed by flow cytometry under resting conditions and after dual agonist stimulation (1 U/mL thrombin + 250 ng/mL convulxin; n = 5)