The roles of alpha IIb beta 3-mediated outside-in signal transduction, thromboxane A2, and adenosine diphosphate in collagen-induced platelet aggregation.
Blood
; 101(7): 2646-51, 2003 Apr 01.
Article
em En
| MEDLINE
| ID: mdl-12446460
ABSTRACT
Collagen-induced activation of platelets in suspension leads to alpha(IIb)beta(3)-mediated outside-in signaling, granule release, thromboxane A2 (TxA2) production, and aggregation. Although much is known about collagen-induced platelet signaling, the roles of TxA2 production, adenosine diphosphate (ADP) and dense-granule secretion, and alpha(IIb)beta(3)-mediated outside-in signaling in this process are unclear. Here, we demonstrate that TxA2 and ADP are required for collagen-induced platelet activation in response to a low, but not a high, level of collagen and that alpha(IIb)beta(3)-mediated outside-in signaling is required, at least in part, for this TxA2 production and ADP secretion. A high level of collagen can activate platelets deficient in PLC gamma 2, G alpha q, or TxA2 receptors, as well as platelets treated with a protein kinase C inhibitor, Ro31-8220. Thus, activation of alpha(IIb)beta(3) in response to a high level of collagen does not require these signaling proteins. Furthermore, a high level of collagen can cause weak TxA2 and ADP-independent aggregation, but maximal aggregation induced by a high level of collagen requires TxA2 or secretion.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Tromboxano A2
/
Transdução de Sinais
/
Difosfato de Adenosina
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Agregação Plaquetária
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Colágeno
/
Complexo Glicoproteico GPIIb-IIIa de Plaquetas
Limite:
Animals
Idioma:
En
Revista:
Blood
Ano de publicação:
2003
Tipo de documento:
Article