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Participation of protein kinases in complement C5b-9-induced shedding of
platelet plasma membrane vesicles
T Wiedmer and PJ Sims
Cardiovascular Biology Research Program, Oklahoma Medical Research
Foundation, Oklahoma City 73104.
The formation of membrane microparticles through vesiculation of the
platelet plasma membrane is known to provide catalytic surface for several
enzyme complexes of the coagulation system, and to underlie the
procoagulant responses elicited with platelet activation. This induced
shedding of vesicles from the plasma membrane is most prominent when
platelets are activated by the terminal complement proteins, C5b-9, by a
Ca2+ ionophore, or by the combination of thrombin plus collagen. Although
shown to require elevated [Ca2+], the cellular events that initiate plasma
membrane evagination and fusion to form the shed vesicles remain
unresolved. To gain additional insight into the cellular events that
regulate membrane microparticle formation, we have examined how this
process is influenced by the activity of cellular protein kinases.
Cytoplasmic [Ca2+] of gel-filtered platelets was increased by membrane
assembly of the terminal complement proteins C5b- 9 in the presence of
selective inhibitors of protein kinase or phosphatase reactions, and
resulting microparticle formation was quantitated by fluorescence-gated
flow cytometry. Pre-equilibration of the phosphatase inhibitor vanadate
into the platelet cytosol increased microparticle formation by as much as
40%, suggesting that vesiculation of the platelet plasma membrane is
influenced by the state of phosphorylation of a cellular constituent. By
contrast to the stimulatory effects of vanadate, microparticle formation
was partially inhibited in platelets treated with the protein kinase
inhibitor sphingosine, the myosin light chain kinase inhibitor ML-7, the
calmodulin-antagonist W-7, and under conditions of elevated cytosolic
concentration of cyclic adenosine monophosphate. These results indicate
that complement-induced platelet microparticle formation is influenced by
one or more protein kinase(s) as well as by calmodulin, and suggest a role
for the platelet myosin light chain kinase or another Ca(2+)-
pluscalmodulin-regulated membrane component.
Volume 78,
Issue 11,
pp. 2880-2886,
12/01/1991
Copyright © 1991 by The American Society of Hematology
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