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Comparison of sea turtle thrombocyte aggregation to human platelet aggregation in whole blood
Journal article

Comparison of sea turtle thrombocyte aggregation to human platelet aggregation in whole blood

Gerald Soslau, Phillip J Prest, Reiner Class, Robert George, Frank Paladino and Gary Violetta
Comparative Biochemistry and Physiology, Part B, v 142(3), pp 353-360
2005
PMID: 16183311

Abstract

Whole blood Thrombocyte aggregation Turtle thrombocytes Hemostasis Human platelet aggregation
The endangered sea turtles are living “fossils” that afford us an opportunity to study the hemostatic process as it likely existed millions of years ago. There are essentially no data about turtle thrombocyte aggregation prior to our studies. Thrombocytes are nucleated cells that serve the same hemostatic functions as the anucleated mammalian platelet. Sea turtle thrombocytes aggregate in response to collagen and β-thrombin. Ristocetin induces an agglutination/aggregation response indicating the presence of a von Willebrand-like receptor, GPIb, found in all mammalian platelets. Samples treated with α-thrombin plus γ-thrombin followed by ristocetin results in a rapid, stronger response than ristocetin alone. These responses are inhibited by the RGDS peptide that blocks fibrinogen cross-linking of mammalian platelets via the fibrinogen receptor, GPIIb/IIIa. Three platelet-like proteins, GPIb, GPIIb/IIIa and P-selection are detected in sea turtle thrombocytes by fluorescence activated cell sorting. Turtle thrombocytes do not respond to ADP, epinephrine, serotonin, thromboxane A 2 mimetic, U46619, trypsin, or α-thrombin and γ-thrombin added alone. Comparison of hemostasis in sea turtles to other vertebrates could provide a framework for understanding the structure/function and evolution of these pathways and their individual components.

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Collaboration types
Domestic collaboration
Web of Science research areas
Biochemistry & Molecular Biology
Zoology
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