Collagen can selectively trigger a platelet secretory phenotype via glycoprotein VI
Autor: | Amena Butt, Angèle Gros, Benoît Ho-Tin-Noé, Stéphane Loyau, Varouna Syvannarath, Martine Jandrot-Perrus, Véronique Ollivier |
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Jazyk: | angličtina |
Rok vydání: | 2014 |
Předmět: |
Platelets
Blood Platelets Integrins Platelet Aggregation Integrin lcsh:Medicine Phosphatidylserines Platelet Membrane Glycoproteins Platelet membrane glycoprotein Antibodies Platelet Adhesiveness Thrombin Medicine and Health Sciences medicine Humans Platelet Calcium Signaling Platelet activation lcsh:Science Blood Coagulation Hemostasis Multidisciplinary biology Chemistry lcsh:R Biology and Life Sciences Thrombosis Cell Biology Hematology Platelet Activation Body Fluids 3. Good health Cell biology P-Selectin Blood Immunology biology.protein lcsh:Q Collagen Anatomy Cellular Types GPVI Platelet factor 4 Research Article medicine.drug |
Zdroj: | PLoS ONE, Vol 9, Iss 8, p e104712 (2014) PLoS ONE |
ISSN: | 1932-6203 |
Popis: | Platelets are not only central actors of hemostasis and thrombosis but also of other processes including inflammation, angiogenesis, and tissue regeneration. Accumulating evidence indicates that these "non classical" functions of platelets do not necessarily rely on their well-known ability to form thrombi upon activation. This suggests the existence of non-thrombotic alternative states of platelets activation. We investigated this possibility through dose-response analysis of thrombin- and collagen-induced changes in platelet phenotype, with regards to morphological and functional markers of platelet activation including shape change, aggregation, P-selectin and phosphatidylserine surface expression, integrin activation, and release of soluble factors. We show that collagen at low dose (0.25 µg/mL) selectively triggers a platelet secretory phenotype characterized by the release of dense- and alpha granule-derived soluble factors without causing any of the other major platelet changes that usually accompany thrombus formation. Using a blocking antibody to glycoprotein VI (GPVI), we further show that this response is mediated by GPVI. Taken together, our results show that platelet activation goes beyond the mechanisms leading to platelet aggregation and also includes alternative platelet phenotypes that might contribute to their thrombus-independent functions. |
Databáze: | OpenAIRE |
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