Role of sialic acid for platelet life span: exposure of beta-galactose results in the rapid clearance of platelets from the circulation by asialoglycoprotein receptor-expressing liver macrophages and hepatocytes. Blood 2009 Aug 20;114(8):1645-54
Date
06/13/2009Pubmed ID
19520807Pubmed Central ID
PMC2731641DOI
10.1182/blood-2009-01-199414Scopus ID
2-s2.0-70349567561 (requires institutional sign-in at Scopus site) 177 CitationsAbstract
Although surface sialic acid is considered a key determinant for the survival of circulating blood cells and glycoproteins, its role in platelet circulation lifetime is not fully clarified. We show that thrombocytopenia in mice deficient in the St3gal4 sialyltransferase gene (St3Gal-IV(-/-) mice) is caused by the recognition of terminal galactose residues exposed on the platelet surface in the absence of sialylation. This results in accelerated platelet clearance by asialoglycoprotein receptor-expressing scavenger cells, a mechanism that was recently shown to induce thrombocytopenia during Streptococcus pneumoniae sepsis. We now identify platelet GPIbalpha as a major counterreceptor on ST3Gal-IV(-/-) platelets for asialoglycoprotein receptors. Moreover, we report data that establish the importance of sialylation of the von Willebrand factor in its function.
Author List
Sørensen AL, Rumjantseva V, Nayeb-Hashemi S, Clausen H, Hartwig JH, Wandall HH, Hoffmeister KMAuthor
Karin Hoffmeister MD Professor in the Biochemistry department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsAsialoglycoprotein Receptor
Blood Platelets
Cell Survival
Cells, Cultured
Female
Galactose
Hepatocytes
Humans
Liver
Macrophages
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
N-Acetylneuraminic Acid
Sialyltransferases
Time Factors
