Regulation of Platelet Function by Orai, STIM and TRP.
Adv Exp Med Biol
; 898: 157-81, 2016.
Article
en En
| MEDLINE
| ID: mdl-27161229
ABSTRACT
Agonist-induced changes in cytosolic Ca(2+) concentration ([Ca(2+)]c) are central events in platelet physiology. A major mechanism supporting agonist-induced Ca(2+) signals is store-operated Ca(2+) entry (SOCE), where the Ca(2+) sensor STIM1 and the channels of the Orai family, as well as TRPC members are the key elements. STIM1-dependent SOCE plays a major role in collagen-stimulated Ca(2+) signaling, phosphatidylserine exposure and thrombin generation. Furthermore, studies involving Orai1 gain-of-function mutants and platelets from Orai1-deficient mice have revealed the importance of this channel in thrombosis and hemostasis to those found in STIM1-deficient mice indicating that SOCE might play a prominent role in thrombus formation. Moreover, increase in TRPC6 expression might lead to thrombosis in humans. The role of STIM1, Orai1 and TRPCs, and thus SOCE, in thrombus formation, suggests that therapies directed against SOCE and targeting these molecules during cardiovascular and cerebrovascular events could significantly improve traditional anti-thrombotic treatments.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Plaquetas
/
Canales de Calcio
/
Canales Catiónicos TRPC
Límite:
Animals
Idioma:
En
Revista:
Adv Exp Med Biol
Año:
2016
Tipo del documento:
Article
País de afiliación:
España