Platelet adhesion, shape change, and aggregation: rapid initiation and signal transduction events

Abstract

GEAR, A.W.L. 1994. Platelet adhesion, shape change, and aggregation: rapid initidion and signal transduction events. Can.J. Physiol. Phamcol. 72: 28% -294. Blood platelets are essential for hemostasis, and knowledge of their function is important for understanding both normal and pathologic situations. A number of approaches have been used to evaluate platelet adhesion, aggregation, and secretion, and within the last Id) years much interest has been directed to the biochemical mechanisms and signal transduction events wcurring during these various phases of function. New information has come from development of technologies to evaluate the changes occurring immediately after platelet activation and consistent with the speed needed for hemostasis in the arterial circulation. Use of rapid flow and mixing technologies as seen in quenched-flow, continuous-flow, and stopped-flow devices has revealed that platelet aggregation, shape change, adhesion, and secretion begin within 1 s and may be nearly complete by 5 s. Biochemical changes such as in protein phosphorylation, calcium release, and phospholipid hydrolysis are clearly evident in hundreds of milliseconds. Therefore, it is necessary to understand these early events in signal transduction and to assess alterations that may occur in diseases such as diabetes.Key rwkards: platelets, quenched flow, aggregation, adhesion, inositol. GEAR,A.R.L. 1994. Platelet adhesion, shape change, and aggregation: rapid initiation and signal transduction events. Can. J. Physiol. Phamacol. 72 : 285-294. Ees plaquettes sanguines jouent un rdle essentiel dans 19hCmostase, et il est important d'en connaitre la fonction pour comprendre tant Ies situations pathologiques que nomales. Plusieurs apprwhes ont Ct C utilisCes pour Cvaluer 19adhCsion, I'agrCgation et B a sCcr6tion des plaquettes, et, au cours des 18 demikres annCes, un intCr6t particulier a Ct C port6 atax mCcanismes biochimiques et B la phase de transduction des signaux dans ces diverses fonctions. De nouvelles informations ont pu Ctre acquises griice au dCveloppement de techniques pour Cvaluer les variations se produisant immCdiatement aprks l'activation plaquettaire et respectant la vitesse nicessaire ? i 19Ctablissement de 1'hCmostase dans la circulation artbrielle. L'utilisation de dCbit mpide et de techniques de knixage qu'offrent les appreils B Ccoulement bioquC, continu ou stoppant, a rCvClC que l'agrdgation, le changement de fome, I'adhCsion et la sCcrCtion des plaquettes commencent en dedans de 1 s et gourraient $tre presque compldt6s en 5 s. k s manifestations biochimiques, observies par exemple dans la phosphorylation protbinique, la libhation de calcium et l'hydrolyse des phospholipides, se prCsentent en qtaelques centaines de millisecondes. Ainsi, il est nCcessaire de comprendre ces phases prCcoces de la transduction des signaux et d'Cvaluer les altkrations qui pourraienmt se produire dans les maladies comme le diabke.

A Model Incorporating Some of the Mechanical and Biochemical Factors Underlying Clot Formation and Dissolution in Flowing Blood

“…The reactions governing the activation of RP by thrombin and by other AP (Reactions 11a and 11b, respectively) follow the kinetics outlined in Kuharsky and Fogelson (2001) (in turn estimated from the data in Gear (1994)). …”

Activators, receptors and signal transduction pathways of blood platelets

“…Клетки сосудистого эндотелия, в случае их повреждении, тоже выбрасывают ADP, содержащийся в них. При добавлении ADP в систему in vitro, тромбоциты начинают синтезировать TXA 2 , это приводит к повышению уровня внутриклеточного Ca 2+ , изменению их формы, происходит фосфорилирование белков, и начинается процесс агрегации тромбоцитов [61], причём агрегируют они тем сильнее, чем больше ADP было добавлено в систему [62]. Таким образом, в случае повреждения сосудистой стенки, некоторое количество тромбоцитов переходят в активированное состояние, и в крови появляется ADP, который может активировать другие тромбоциты.…”

Trombosi̇t Akti̇vasyonu

“…TxA2 trombosit membranı üzerindeki reseptö-rüne bağlanarak trombosit aktivasyonuna 'yol açar (4,5,6,7,8,9).…”