Uneyama C, Imazawa T, Uneyama H, Akaike N, Kawanishi T, Takahashi M
Division of Pathology, National Institute of Health Sciences, Tokyo, Japan.
Biochem Biophys Res Commun. 1995 Jun 6;211(1):282-8. doi: 10.1006/bbrc.1995.1808.
ATP and thrombin both induced Ca2+ mobilization from intracellular Ca2+ store site of megakaryocyte, the progenitor cell of platelet (Uneyama C., Uneyama H. and Akaike N. (1993) J. Physiol. (Lond.), 470, 73-749). Since in platelet, thrombin is known as a strong agonist and ADP is known as a weak agonist, we further investigated the effect of these agonists on megakaryocyte. Thrombin induced Ca2+ mobilization, 5-hydroxy tryptamine (5-HT) release and aggregatory morphological changes in megakaryocyte, but ATP induced only Ca2+ mobilization. Thrombin-induced 5-HT release was inhibited by adenylate cyclase-activating drugs, and the morphological changes could be induced by H-8, an inhibitor of cAMP-dependent protein kinase. These results suggest that the Ca2+ mobilization is not sufficient to induce morphological changes, and the signal to cause morphological changes in megakaryocyte may be cAMP.
ATP和凝血酶均可诱导血小板祖细胞巨核细胞内Ca2+从细胞内Ca2+储存位点动员出来(Uneyama C.、Uneyama H.和Akaike N.(1993年)《生理学杂志》(伦敦),470,73 - 749)。由于在血小板中,凝血酶是一种强激动剂,而ADP是一种弱激动剂,我们进一步研究了这些激动剂对巨核细胞的影响。凝血酶可诱导巨核细胞内Ca2+动员、5-羟色胺(5-HT)释放和聚集性形态变化,但ATP仅诱导Ca2+动员。腺苷酸环化酶激活药物可抑制凝血酶诱导的5-HT释放,而形态变化可由cAMP依赖性蛋白激酶抑制剂H-8诱导。这些结果表明,Ca2+动员不足以诱导形态变化,而导致巨核细胞形态变化的信号可能是cAMP。