Affiliation:
1. From the Department of Surgery, Beth Israel Hospital, Harvard Medical School, Boston, Mass.
Abstract
Abstract
We monitored the intracellular distribution of ionized free Ca
2+
concentration ([Ca
2+
]
i
) in individual human platelets by digital imaging fluorescence microscopy with fura 2 during platelet activation induced by surface contact or a soluble platelet agonist (thrombin). Contact of platelets with glass resulted in pseudopod formation and spreading, accompanied by a nonuniform rise in [Ca
2+
]
i
. The rise in [Ca
2+
]
i
was maximal during pseudopod formation. Locally elevated [Ca
2+
]
i
was frequently found in pseudopodia and at the edge and core of spread platelets. This pattern was faithfully duplicated by the local pattern of distribution of the cytoskeletal components F-actin, gelsolin, and surface glycoproteins (GP) IIb-IIIa but not by calmodulin. Platelets stimulated by thrombin also showed an inhomogeneous rise in [Ca
2+
]
i
, which was well correlated with the staining of F-actin and GPIIb-IIIa. Cytochalasin D, an inhibitor of actin polymerization, inhibited the inhomogeneous increase or redistribution of F-actin and GPIIb-IIIa but did not inhibit the rise in mean [Ca
2+
]
i
. These observations suggest that a localized change in [Ca
2+
]
i
may be associated with cytoskeletal reorganization and redistribution of GPIIb-IIIa in activated platelets.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine
Cited by
20 articles.
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