PB0869 - Platelet-derived microvesicles have a reparative role for muscle damage induced by hypothermia

Monday, June 26, 2023

18:30 – 19:30 ET

Room: Exhibition

Presenting Author(s)

Kie Horioka, PhD

Postdoctoral fellow
Department of Forensic Medicine, Research Unit of Internal Medicine, Medical Research Center Oulu, University of Oulu
Oulu, Pohjois-Pohjanmaa, Finland

Co-Author(s)

Hiroki Tanaka

Assistant professor
Department of Pathology, Division of Tumor Pathology
Asahikawa, Hokkaido, Japan
AH

Akira Hayakawa

Lecturer
Department of Legal Medicine, Gunma University Graduate School of Medicine
Maebashi, Gumma, Japan
LP

Lasse Pakanen

Research group leader
Department of Forensic Medicine, Research Unit of Internal Medicine, Medical Research Center Oulu,University of Oulu
Oulu, Pohjois-Pohjanmaa, Finland
KP

Katja Porvari

Docent
Department of Forensic Medicine, Research Unit of Internal Medicine, Medical Research Center Oulu,University of Oulu
Oulu, Pohjois-Pohjanmaa, Finland

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.

Aims: 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 until 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 control mice. Electron microscopy and real-time RT-PCR analysis revealed that platelets activated in the spleen by hypothermia internalized e.g., 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 hours after rewarming. However, splenectomy delayed recovery from skeletal muscle injury after the mice were rewarmed.

Conclusion(s): 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.