Impact of shear stress on Src and focal adhesion kinase phosphorylation in fibrinogen-adherent platelets.
Blood Coagul Fibrinolysis
; 28(4): 279-285, 2017 Jun.
Article
em En
| MEDLINE
| ID: mdl-27467982
ABSTRACT
Shear stress alone can activate platelets resulting in a subsequent platelet aggregation, so-called 'shear-induced platelet aggregation'. In our work, we analyzed how differently elevated shear stress impacts the Src and focal adhesion kinase (FAK) activation in fibrinogen-adherent human platelets. We detected the extents of Src pY418 and FAK pY397 activations in platelets on immobilized fibrinogen and over BSA under shear conditions. Moreover, we analyzed the role of αIIbß3 in the shear-induced platelet signaling by performing our experiments in the presence of the αIIbß3-antagonist Abciximab. Abnormally high shear rates (5000âs) significantly increased the extent of phosphorylation of both tyrosine kinases after short (2âmin) incubation time independently of the presence or absence of the integrin αIIbß3 ligand, fibrinogen. We could see considerably greater Src activation on immobilized fibrinogen than on BSA, but the extent of FAK Y397 phosphorylation was independent on the matrix. Abciximab not only reduced the Src and FAK signaling in platelets exposed to 5000âs on immobilized fibrinogen, but in platelets exposed to 5000âs over BSA as well. Our data indicate that whereas Src activation under shear stress is dominantly ligand-dependent, FAK signaling seems to be mostly shear induced.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Estresse Mecânico
/
Plaquetas
/
Fibrinogênio
/
Adesividade Plaquetária
/
Proteínas Proto-Oncogênicas pp60(c-src)
/
Proteína-Tirosina Quinases de Adesão Focal
Limite:
Humans
Idioma:
En
Revista:
Blood Coagul Fibrinolysis
Assunto da revista:
ANGIOLOGIA
/
HEMATOLOGIA
Ano de publicação:
2017
Tipo de documento:
Article
País de afiliação:
Alemanha