Mukherjee G, Chatterjee G C, Banerjee D, Bhattacharya D K
Department of Biochemistry, University College of Science, Calcutta, India.
Indian J Exp Biol. 1990 Oct;28(10):949-52.
Retinoic acid (RA) was found to inhibit ADP induced but not collagen induced aggregation of human platelets and the differential action is related to intraplatelet Ca2+ reflux. RA was active at concentrations as low as 10(-7) M and required 20 min prior incubation with platelet suspension in order to inhibit aggregation by ADP. All the steps in ADP induced but not collagen induced platelet activation, viz. hydrolysis of phosphatidyl inositol, phosphorylation of 20, 47 and 250 kDa proteins as well as increased association of actin with Triton X-100 insoluble cytoskeletal matrix were inhibited by RA. RA when used as an agent for differentiation induction of cell progenitor is likely to affect the platelet aggregation and thereby the haemostatic process.
维甲酸（RA）被发现可抑制二磷酸腺苷（ADP）诱导的人血小板聚集，但不抑制胶原蛋白诱导的聚集，且这种差异作用与血小板内钙离子回流有关。RA在低至10^(-7) M的浓度下就有活性，并且需要在与血小板悬液预孵育20分钟后才能抑制ADP诱导的聚集。ADP诱导的但不是胶原蛋白诱导的血小板活化的所有步骤，即磷脂酰肌醇的水解、20 kDa、47 kDa和250 kDa蛋白质的磷酸化以及肌动蛋白与Triton X-100不溶性细胞骨架基质的结合增加，均被RA抑制。当RA用作细胞祖细胞分化诱导剂时，可能会影响血小板聚集，从而影响止血过程。
