Ken-Ichi Furukawa (1), Mika Matsuzawa (1), Susumu Tsurufuji (2), Kazuyoshi
Watanabe (2) and Yasushi Ohizumi (1)
(1) Department of Pharmaceutical Molecular Biology, Faculty of Pharmaceutical Sciences, Tohoku University, Aoba, Aramaki, Aoba-ku, Sendai 980, Japan
(2) Institute of Cytosignal Research, Hiromachi 1-2-58, Shinagawa-ku, Tokyo 140, Japan
Abstract: 2,5-Di-(tert-butyl)-1,4-benzohydroquinone (tBuBHQ), an inhibitor of endoplasmic reticulum Ca2+-ATPase, caused aggregation accompanied by a marked increase in intracellular Ca2+ concentrations ([Ca2+]i) in washed rabbit platelets. Treatment of platelets with SK&F96365 or removal of extracellular Ca2+ inhibited both Ca2+ influx and platelet aggregation induced by tBuBHQ. These responses of platelets to tBuBHQ were also inhibited by genistein. Western blots using antibody against phosphorylated amino acid residues revealed that tBuBHQ activated tyrosine kinase independently of extracellular Ca2+. These results suggest that tBuBHQ induces Ca2+ influx into platelets probably through activation of tyrosine kinase, resulting in platelet aggregation.
Keywords: Platelet aggregation, 2,5-Di-(tert-butyl)-1,4-benzohydroquinone, Tyrosine kinase