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Zinc (Zn 2+ ) can modulate platelet and coagulation activation pathways, including fibrin formation. Here, we studied the (patho)physiological consequences of abnormal platelet Zn 2+  storage and release. To visualize Zn 2+  storage in human and mouse platelets, the Zn 2+  specific fluorescent dye FluoZin3 was used. In resting platelets, the dye transiently accumulated into distinct cytosolic puncta, which were lost upon platelet activation. Platelets isolated from  Unc13d  −/−  mice, characterized by combined defects of α/δ granular release, showed a markedly impaired Zn 2+  release upon activation. Platelets from  Nbeal2  −/−  mice mimicking Gray platelet syndrome (GPS), characterized by primarily loss of the α-granule content, had strongly reduced Zn 2+  levels, which was also confirmed in primary megakaryocytes. In human platelets isolated from patients with GPS, Hermansky-Pudlak Syndrome (HPS) and Storage Pool Disease (SPD) altered Zn 2+  homeostasis was detected. In turbidity and flow based assays, platelet-dependent fibrin formation was impaired in both  Nbeal2  −/−  and  Unc13d  −/−  mice, and the impairment could be partially restored by extracellular Zn 2+ . Altogether, we conclude that the release of ionic Zn 2+  store from secretory granules upon platelet activation contributes to the procoagulant role of Zn 2+  in platelet-dependent fibrin formation.

Defective Zn2+ homeostasis in mouse and human platelets with α- and δ-storage pool diseases