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BA Fiedel
C-reactive protein is the prototypic acute phase reactant. A self-
complexed form (H-CRP) can induce isolated platelets to undergo
aggregation, secretion of dense and alpha-granule constituents, and
generation of thromboxane A2, but fails to function in platelet-rich plasma
(PRP) as a direct agonist. In contrast, when PRP was activated with an
amount of adenosine diphosphate (ADP) that produced only reversible
platelet aggregation, the presence of H-CRP resulted in irreversible
aggregation and the secretion of adenosine triphosphate (ATP). Following a
maximum stimulus with ADP alone, where platelet secretion occurred late
during the aggregation response, the presence of H-CRP shifted and
increased the secretory burst to a time simultaneous with the onset of
aggregation. This hypersecretion required H-CRP to be present prior to
platelet stimulation or to be added within 15 to 30 seconds following the
addition of ADP. H-CRP also potentiated platelet activation stimulated with
epinephrine, thrombin, and collagen. When the synergism generated in PRP by
H-CRP in the presence of ADP or epinephrine was compared to the synergism
similarly produced by aggregated human IgG, collagen, or thrombin, it more
closely resembled that of collagen, as reflected by the kinetics and
characteristics of synergism and sensitivity to creatine phosphate/creatine
phosphokinase or 5,8,11,14-eicosatetraynoic acid. These data provide a
philosophically ideal niche for the acute phase (and C-reactive protein) in
that a platelet-directed activity associated with this acute phase reactant
is not utilized unless platelets are otherwise challenged.
This article has been cited by other articles:
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| Copyright © 1985 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
