Involvement of Gi/o in the PAR-4-induced NO production in endothelial cells

Fumi Momota, Katsuya Hirano, Mayumi Hirano, Junji Nishimura, Hideo Kanaide

研究成果: ジャーナルへの寄稿学術誌査読

12 被引用数 (Scopus)


We investigated the involvement of Gi/o protein in NO production following the activation of proteinase-activated receptor-4 (PAR-4) in cultured bovine aortic endothelial cells. AYPGKF-NH2 (PAR-4 activating peptide), thrombin, and ionomycin induced a concentration-dependent NO production, with the maximal production seen at 30 μM, 0.1 U/ml, and 1 μM, respectively. Ionomycin elevated [Ca2+]i in a concentration-dependent manner. However, AYPGKF-NH2 and thrombin induced no [Ca2+]i elevation. The loading of cells with BAPTA almost completely inhibited both the NO production and [Ca 2+]i elevation induced by 1 μM ionomycin, while it had no significant effect on the AYPGKF-NH2-induced NO production. Treatment with pertussis toxin inhibited the AYPGKF-NH2-induced NO production, while it had no effect on the ionomycin-induced NO production. Our findings thus demonstrate, for the first time, that PAR-4 activation induced NO production in a manner mostly independent of the Ca2+ signal and also that Gi/o is involved in such NO production in vascular endothelial cells.

ジャーナルBiochemical and Biophysical Research Communications
出版ステータス出版済み - 4月 7 2006

!!!All Science Journal Classification (ASJC) codes

  • 生物理学
  • 生化学
  • 分子生物学
  • 細胞生物学


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