Why the study?
Does collagen induce normal signal transduction in platelets deficient in CD36?
Does collagen induce normal signal transduction in platelets deficient in CD36?
CD36 does not appear to play a major role in collagen-dependent platelet signal transduction.
CD36 appears dispensable for collagen signaling in this animal model; leaves open its relevance to human platelet function and thrombosis.
The receptor involved in platelet activation by collagen has not been identified. Platelet glycoprotein IV, now known as CD36, has been implicated in interaction with collagen and also been shown to be associated with intracellular tyrosine kinases. In order to investigate the possible role of collagen-mediated signal transduction via CD36, platelets were obtained from a donor that were deficient in CD36. The collagen-induced intracellular mobilization of Ca2+ in the CD36 deficient cells was of the same magnitude as that seen in platelets from normal donors. In addition, serotonin secretion did not appear to be impaired. Tyrosine phosphorylation was also comparable between the CD36-deficient and normal platelets. Thus, it is unlikely that CD36 plays a major role in collagen-dependent platelet signal transduction.
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Daniel et al. (1994) studied this question.
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