Arachidonic acid uptake by human platelets is mediated by CD36
作者:
DuttaA. K.,
GordonM. J.,
CampbellF. M.,
CrosbieL. C.,
期刊:
Platelets
(Taylor Available online 1996)
卷期:
Volume 7,
issue 5-6
页码: 291-295
ISSN:0953-7104
年代: 1996
DOI:10.3109/09537109609023591
出版商: Taylor&Francis
数据来源: Taylor
摘要:
The involvement of glycoprotein (GP) IV (CD36) in arachidonic acid uptake by human platelets was investigated using an anti-CD36 monoclonal antibody (MAB). The binding of [14C]arachidonic acid to MAB-treated platelets was significantly reduced compared with untreated platelets. The MAB also inhibited arachidonic acid-induced platelet aggregation and thromboxane A2synthesis in a dose-dependent manner. Pre-incubation of gel-filtered platelets with the MAB (10mg/I) inhibited arachidonic acid-induced platelet aggregation by 50% and collagen-induced platelet aggregation by 7-8% and the lag time was increased by 200%. Although the mechanism of platelet aggregation is not fully understood yet, the inhibition of arachidonic acid-induced platelet aggregation by the MAB could be the result of a reduced uptake of exogeneously added arachidonic acid by the MAB-treated platelets. Our data clearly indicate that arachidonic acid uptake by platelets is mediated, at least in part, by CD36.
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