Staphylococcal superantigen-like 5 activates platelets and supports platelet adhesion under flow conditions, which involves glycoprotein Ib alpha and alpha(IIb)beta(3)
| Autor: | Ton Lisman, Mignon M. Vughs, de Peter Groot, C. J. C. de Haas, Cees Weeterings, J. A. G. Van Strijp |
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| Přispěvatelé: | Groningen Institute for Organ Transplantation (GIOT), Vascular Ageing Programme (VAP) |
| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
Blood Platelets
Erythrocytes P-selectin Platelet Aggregation Staphylococcus IMMUNE EVASION PROTEIN COUNTERRECEPTOR Platelet Glycoprotein GPIIb-IIIa Complex THROMBIN aureus GPIb alpha Platelet Adhesiveness AUREUS INFECTIONS Platelet adhesiveness BINDING Platelet Platelet activation Cells Cultured Superantigens biology Chemistry P-SELECTIN IX-V COMPLEX Platelet Glycoprotein GPIb-IX Complex Hematology flow conditions SSL5 DIMERIC BETA(2)-GLYCOPROTEIN-I AGGREGATION Platelet Activation Cell biology Endothelial stem cell Perfusion Biochemistry Glycoprotein Ib platelets biology.protein |
| Zdroj: | Journal of Thrombosis and Haemostasis, 7(11), 1867-1874. Wiley |
| ISSN: | 1538-7933 |
| Popis: | Objectives: Staphylococcal superantigen-like 5 (SSL5) is an exoprotein secreted by Staphylococcus aureus that has been shown to inhibit neutrophil rolling over activated endothelial cells via a direct interaction with P-selectin glycoprotein ligand 1 (PSGL-1). Methods and Results: When purified recombinant SSL5 was added to washed platelets in an aggregometry set-up, complete and irreversible aggregation was observed. Proteolysis of the extracellular part of GPIb alpha or the addition of dRGDW abrogated platelet aggregation. When a mixture of isolated platelets and red cells was perfused over immobilized SSL5 at a shear rate of 300 s-1, stable platelet aggregates were observed, and platelet deposition was substantially reduced after proteolysis of GPIb or after addition of dRGDW. SSL5 was shown to interact with glycocalicin, a soluble GPIb alpha fragment, and binding of SSL5 to platelets resulted in GPIb-mediated signal transduction as evidenced by translocation of 14-3-3 zeta. In addition, SSL5 was shown to interact with endothelial cell matrix (ECM) and this interaction enhanced aggregation of platelets from whole blood to this ECM. Conclusions: SSL5 activates and aggregates platelets in a GPIb alpha-dependent manner, which could be important in colonization of the vascular bed and evasion of the immune system by S. aureus. |
| Databáze: | OpenAIRE |
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