Actin dynamics in platelets.
The human blood platelet circulates in the blood as a non-adherent disk. Upon receiving signals of blood vessel damage, the platelet reorganizes its actin cytoskeleton which transforms it into a spiky dynamic adherent glue. This transformation involves a temporal sequence of four morphologically distinct steps which is reproducible in vitro. The actin dynamics underlying these shape changes depend on a large number of actin-binding proteins. Maintenance of the discoid shape requires actin-binding proteins that inhibit these reorganizations, whereas transformation involves other proteins, some to disassemble old filaments and others to polymerize new ones. F-Actin-affinity chromatography identified a large set of actin-binding proteins including VASP, Arp2 and 2E4/kaptin. Recent discoveries show that VASP inhibits filament disassembly and Arp2/3 is required to polymerize new filaments. Morphological analysis of the distribution of these actin-binding proteins in spread platelets together with biochemical measurements of their interactions with actin lead to a model of interactions with actin that mediate shape change.
Bearer
E L
EL
Department of Pathology and Laboratory Medicine, Brown University, Providence, Rhode Island 02912, USA.
Prakash
J M
JM
Li
Z
Z
D000199:Actins / Q000378:metabolism* / Q000502:physiology; D000818:Animals; D001792:Blood Platelets / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D002118:Calcium / Q000378:metabolism; D003593:Cytoplasm / Q000378:metabolism; D006801:Humans; D015539:Platelet Activation; D013997:Time Factors
D000199:Actins; D002118:Calcium