抄録
We investigated the involvement of G i/o protein in NO production following the activation of proteinase-activated receptor-4 (PAR-4) in cultured bovine aortic endothelial cells. AYPGKF-NH 2 (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 [Ca 2+ ] i in a concentration-dependent manner. However, AYPGKF-NH 2 and thrombin induced no [Ca 2+ ] 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-NH 2 -induced NO production. Treatment with pertussis toxin inhibited the AYPGKF-NH 2 -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 Ca 2+ signal and also that G i/o is involved in such NO production in vascular endothelial cells.
| 元の言語 | 英語 |
|---|---|
| ページ（範囲） | 365-371 |
| ページ数 | 7 |
| ジャーナル | Biochemical and Biophysical Research Communications |
| 巻 | 342 |
| 発行部数 | 2 |
| DOI | |
| 出版物ステータス | 出版済み - 4 7 2006 |
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All Science Journal Classification (ASJC) codes
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology
これを引用
Involvement of G i/o in the PAR-4-induced NO production in endothelial cells . / Momota, Fumi; Hirano, Katsuya; Hirano, Mayumi; Nishimura, Junji; Kanaide, Hideo.
：: Biochemical and Biophysical Research Communications, 巻 342, 番号 2, 07.04.2006, p. 365-371.研究成果: ジャーナルへの寄稿 › 記事
}
TY - JOUR
T1 - Involvement of G i/o in the PAR-4-induced NO production in endothelial cells
AU - Momota, Fumi
AU - Hirano, Katsuya
AU - Hirano, Mayumi
AU - Nishimura, Junji
AU - Kanaide, Hideo
PY - 2006/4/7
Y1 - 2006/4/7
N2 - We investigated the involvement of G i/o protein in NO production following the activation of proteinase-activated receptor-4 (PAR-4) in cultured bovine aortic endothelial cells. AYPGKF-NH 2 (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 [Ca 2+ ] i in a concentration-dependent manner. However, AYPGKF-NH 2 and thrombin induced no [Ca 2+ ] 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-NH 2 -induced NO production. Treatment with pertussis toxin inhibited the AYPGKF-NH 2 -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 Ca 2+ signal and also that G i/o is involved in such NO production in vascular endothelial cells.
AB - We investigated the involvement of G i/o protein in NO production following the activation of proteinase-activated receptor-4 (PAR-4) in cultured bovine aortic endothelial cells. AYPGKF-NH 2 (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 [Ca 2+ ] i in a concentration-dependent manner. However, AYPGKF-NH 2 and thrombin induced no [Ca 2+ ] 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-NH 2 -induced NO production. Treatment with pertussis toxin inhibited the AYPGKF-NH 2 -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 Ca 2+ signal and also that G i/o is involved in such NO production in vascular endothelial cells.
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UR - http://www.scopus.com/inward/citedby.url?scp=33344472078&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2006.01.165
DO - 10.1016/j.bbrc.2006.01.165
M3 - Article
VL - 342
SP - 365
EP - 371
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 2
ER -