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Beta 3 integrin-mediated fibrin clot retraction by nucleated cells:
differing behavior of alpha IIb beta 3 and alpha v beta 3
YP Chen, TE O'Toole, L Leong, BQ Liu, F Diaz-Gonzalez and MH Ginsberg
Department of Vascular Biology, Scripps Research Institute, La Jolla, CA
92037, USA.
Fibrin clot retraction may be important in resolution of thrombi and, in
platelets, is mediated by integrin alpha IIb beta 3 (GPIIb-IIIa). Nucleated
cells that lack alpha IIb beta 3 can retract fibrin clots, and we now
report that integrin alpha v beta 3 can support this process. In addition,
we compared the capacities of recombinant beta 3 integrins to mediate clot
retraction in Chinese hamster ovary and M21 melanoma cells. We found that
alpha v beta 3, but not alpha IIb beta 3, could spontaneously support
retraction. Transferring the cytoplasmic domain of alpha v to alpha IIb
enabled the resulting chimeric alpha IIb beta 3 to support clot retraction.
The capacity of the alpha v cytoplasmic domain to support clot retraction
was not caused by activation of the ligand binding function of alpha IIb
beta 3 or by enhancement of alpha IIb beta 3's capacity to stimulate the
formation of focal adhesions or the tyrosine phosphorylation of pp125FAK.
These experiments define requirements for alpha IIb beta 3-mediating clot
retraction, establish the capacity of alpha v beta 3 to mediate this
process, and suggest differing functional roles of the alpha v and alpha
IIb cytoplasmic domains.
Volume 86,
Issue 7,
pp. 2606-2615,
10/01/1995
Copyright © 1995 by The American Society of Hematology
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