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Background: Most platelets are present in peripheral blood, but some are stored in the spleen. Because the tissue environments of peripheral blood vessels and the spleen are quite distinct, the properties of platelets present in each may also differ. However, no studies have addressed this difference. We previously reported that hypothermia activates splenic platelets, but not peripheral blood platelets, whose biological significance remains unknown. In this study, we focused on platelet-derived microvesicles (PDMVs) and analyzed their biological significance connected to intrasplenic platelet activation during hypothermia., Methods: C57Bl/6 mice were placed in an environment of -20 °C, and their rectal temperature was decreased to 15 °C to model hypothermia. Platelets and skeletal muscle tissue were collected and analyzed for their interactions., Results: Transcriptomic changes between splenic and peripheral platelets were greater in hypothermic mice than in normal mice. Electron microscopy and real-time RT-PCR analysis revealed that platelets activated in the spleen by hypothermia internalized transcripts, encoding tissue repairing proteins, into PDMVs and released them into the plasma. Plasma microvesicles from hypothermic mice promoted wound healing in the mouse myoblast cell line C2C12. Skeletal muscles in hypothermic mice were damaged but recovered within 24 h after rewarming. However, splenectomy delayed recovery from skeletal muscle injury after the mice were rewarmed., Conclusions: These results indicate that PDMVs released from activated platelets in the spleen play an important role in the repair of skeletal muscle damaged by hypothermia., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: Accidental hypothermia results in various dysfunctions in the human body. Additionally, coagulation disorder can lead to a life-threatening condition. We previously demonstrated that platelets stored in the spleen were activated and thus triggered coagulation disorder in a mouse model of hypothermia. In the present study, we wanted to investigate if this phenomenon in mice also occurs in humans as a reaction to hypothermia., Methods: We analyzed splenic tissue collected from 22 deceased subjects who have died from hypothermia. These samples were compared with 22 control cases not exposed to cold environment. We performed immunohistochemical staining for CD61 (a marker of all platelets) and CD62P (a marker of activated platelets). We also evaluated the morphology of platelets in the spleen with scanning electron microscopy., Results: Immunohistochemical analysis revealed no significant changes in the amounts of CD61-positive platelets between the hypothermia and control cases. However, the hypothermia cases contained abundant CD62P-positive platelets compared with those of the control cases. Immunohistochemical analysis also revealed that the activated platelets formed aggregates and adhered to splenic sinusoidal endothelial cells in the hypothermia cases. However, we observed no significant fibrin formation around the activated platelets., Conclusions: Hypothermia resulted in splenic platelet activation, which may be used as a postmortem marker of hypothermia. The release of activated platelets from the spleen into to circulation upon rewarming may promote coagulation disturbances., (Copyright © 2021 Elsevier Ltd. All rights reserved.)