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