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. Author manuscript; available in PMC: 2017 Sep 1.
Published in final edited form as: Platelets. 2016 May 2;27(6):505–511. doi: 10.3109/09537104.2016.1171304

Figure 2. In vivo and in vitro platelet aging.

Figure 2

(A) Senescent platelets lose sialic acid while circulating leading to exposure of penultimate surface galactose. Desialylated platelets bind to the hepatic Ashwell-Morell Receptor (AMR) on hepatocytes to initiate the JAK2-STAT3 signaling cascade and thrombopoietin (TPO) production to regulate steady state platelet numbers. (B) Platelets stored at 4°C lose both sialic acid and galactose and are cleared by the AMR on hepatocytes and the αMβ2 integrin (via its αM subunit lectin domain) on hepatic macrophages (Kupffer cells). It remains to be determined if engagement of cold stored platelets with either receptor induces intracellular signaling.