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- W4210361330 abstract "Platelet transfusion is a very common lifesaving medical procedure. Not widely known is the fact that platelets, unlike other blood cells, rapidly leave the circulation if refrigerated prior to transfusion. This peculiarity requires blood services to store platelets at room temperature, limiting platelet supplies for clinical needs. Here, we describe the mechanism of this clearance system, a longstanding mystery. Chilling platelets clusters their von Willebrand (vWf) receptors, eliciting recognition of mouse and human platelets by hepatic macrophage complement type 3 (CR3) receptors. CR3-expressing but not CR3-deficient mice exposed to cold rapidly decrease platelet counts. Cooling primes platelets for activation. We propose that platelets are thermosensors, primed at peripheral sites where most injuries occurred throughout evolution. Clearance prevents pathologic thrombosis by primed platelets. Chilled platelets bind vWf and function normally in vitro and ex vivo after transfusion into CR3-deficient mice. Therefore, GPIb modification might permit cold platelet storage. PMID: 12526796 Funding information This work was supported by: NHLBI NIH HHS, United States Grant ID: HL56949 NHLBI NIH HHS, United States Grant ID: HL36028 NHLBI NIH HHS, United States Grant ID: HL19429 NHLBI NIH HHS, United States Grant ID: P01 HL056949" @default.
- W4210361330 created "2022-02-08" @default.
- W4210361330 creator A5032907445 @default.
- W4210361330 date "2003-03-29" @default.
- W4210361330 modified "2023-09-27" @default.
- W4210361330 title "Faculty Opinions recommendation of The clearance mechanism of chilled blood platelets." @default.
- W4210361330 doi "https://doi.org/10.3410/f.1009772.186895" @default.
- W4210361330 hasPublicationYear "2003" @default.
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