Endogenous NO blockade enhances tissue factor expression via increased Ca2+ influx through MCP-1 in endothelial cells by monocyte adhesion

Takayuki Sakamoto, Toshiyuki Ishibashi, Nobuo Sakamoto, Koichi Sugimoto, Kensuke Egashira, Hiroshi Ohkawara, Kenji Nagata, Keiko Yokoyama, Masashi Kamioka, Toshihiro Ichiki, Naotoshi Sugimoto, Masahiko Kurabayashi, Koji Suzuki, Yoh Takuwa, Yukio Maruyama

研究成果: ジャーナルへの寄稿記事

27 引用 (Scopus)

抄録

Objective - Ca2+ plays an important role in tissue factor (TF) gene expression. We investigated the role of endogenous nitric oxide (NO) in the induction of TF expression in endothelial cells (ECs) by monocyte adhesion and the mechanisms of NO action. Methods and Results - Inhibition of endogenous NO by Nω-nitro-L-arginine methyl ester (L-NAME) enhanced TF promoter activity and protein expression induced in human coronary ECs by monocyte adhesion, as well as EC surface TF activity. L-NAME also induced monocyte chemoattractant protein-1 (MCP-1) expression, which was blocked by an NO donor, NOC18. Exogenous MCP-1 enhanced TF expression induced by monocyte adhesion, whereas adenovirus-mediated expression of the mutant MCP-1, 7ND, abolished the L-NAME enhancement of TF expression induced by monocyte adhesion. Monocyte attachment to L-NAME-treated ECs increased Ca2+ influx, which was prevented by NOC18, anti-MCP-1 antibody or 7ND. These results indicate that the binding of increased MCP-1 induced by endogenous NO blockade to CCR2 mediated the enhancement of Ca2+ influx only when monocytes adhered to ECs, which upregulated TF expression in ECs triggered by monocyte adhesion. Conclusion - MCP-1/CCR2 may play a role in Ca2+ influx-dependent TF regulation in the monocyte-EC interaction in the impairment of NO synthesis.

元の言語英語
ページ(範囲)2005-2011
ページ数7
ジャーナルArteriosclerosis, thrombosis, and vascular biology
25
発行部数9
DOI
出版物ステータス出版済み - 9 1 2005

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Chemokine CCL2
Thromboplastin
Cell Adhesion
Monocytes
Nitric Oxide
Endothelial Cells
NG-Nitroarginine Methyl Ester
Nitric Oxide Donors
Mutant Proteins
Adenoviridae
Cell Communication
Gene Expression
Antibodies

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

これを引用

Endogenous NO blockade enhances tissue factor expression via increased Ca2+ influx through MCP-1 in endothelial cells by monocyte adhesion. / Sakamoto, Takayuki; Ishibashi, Toshiyuki; Sakamoto, Nobuo; Sugimoto, Koichi; Egashira, Kensuke; Ohkawara, Hiroshi; Nagata, Kenji; Yokoyama, Keiko; Kamioka, Masashi; Ichiki, Toshihiro; Sugimoto, Naotoshi; Kurabayashi, Masahiko; Suzuki, Koji; Takuwa, Yoh; Maruyama, Yukio.

:: Arteriosclerosis, thrombosis, and vascular biology, 巻 25, 番号 9, 01.09.2005, p. 2005-2011.

研究成果: ジャーナルへの寄稿記事

Sakamoto, T, Ishibashi, T, Sakamoto, N, Sugimoto, K, Egashira, K, Ohkawara, H, Nagata, K, Yokoyama, K, Kamioka, M, Ichiki, T, Sugimoto, N, Kurabayashi, M, Suzuki, K, Takuwa, Y & Maruyama, Y 2005, 'Endogenous NO blockade enhances tissue factor expression via increased Ca2+ influx through MCP-1 in endothelial cells by monocyte adhesion', Arteriosclerosis, thrombosis, and vascular biology, 巻. 25, 番号 9, pp. 2005-2011. https://doi.org/10.1161/01.ATV.0000178171.61754.cd
Sakamoto, Takayuki ; Ishibashi, Toshiyuki ; Sakamoto, Nobuo ; Sugimoto, Koichi ; Egashira, Kensuke ; Ohkawara, Hiroshi ; Nagata, Kenji ; Yokoyama, Keiko ; Kamioka, Masashi ; Ichiki, Toshihiro ; Sugimoto, Naotoshi ; Kurabayashi, Masahiko ; Suzuki, Koji ; Takuwa, Yoh ; Maruyama, Yukio. / Endogenous NO blockade enhances tissue factor expression via increased Ca2+ influx through MCP-1 in endothelial cells by monocyte adhesion. :: Arteriosclerosis, thrombosis, and vascular biology. 2005 ; 巻 25, 番号 9. pp. 2005-2011.
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abstract = "Objective - Ca2+ plays an important role in tissue factor (TF) gene expression. We investigated the role of endogenous nitric oxide (NO) in the induction of TF expression in endothelial cells (ECs) by monocyte adhesion and the mechanisms of NO action. Methods and Results - Inhibition of endogenous NO by Nω-nitro-L-arginine methyl ester (L-NAME) enhanced TF promoter activity and protein expression induced in human coronary ECs by monocyte adhesion, as well as EC surface TF activity. L-NAME also induced monocyte chemoattractant protein-1 (MCP-1) expression, which was blocked by an NO donor, NOC18. Exogenous MCP-1 enhanced TF expression induced by monocyte adhesion, whereas adenovirus-mediated expression of the mutant MCP-1, 7ND, abolished the L-NAME enhancement of TF expression induced by monocyte adhesion. Monocyte attachment to L-NAME-treated ECs increased Ca2+ influx, which was prevented by NOC18, anti-MCP-1 antibody or 7ND. These results indicate that the binding of increased MCP-1 induced by endogenous NO blockade to CCR2 mediated the enhancement of Ca2+ influx only when monocytes adhered to ECs, which upregulated TF expression in ECs triggered by monocyte adhesion. Conclusion - MCP-1/CCR2 may play a role in Ca2+ influx-dependent TF regulation in the monocyte-EC interaction in the impairment of NO synthesis.",
author = "Takayuki Sakamoto and Toshiyuki Ishibashi and Nobuo Sakamoto and Koichi Sugimoto and Kensuke Egashira and Hiroshi Ohkawara and Kenji Nagata and Keiko Yokoyama and Masashi Kamioka and Toshihiro Ichiki and Naotoshi Sugimoto and Masahiko Kurabayashi and Koji Suzuki and Yoh Takuwa and Yukio Maruyama",
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T1 - Endogenous NO blockade enhances tissue factor expression via increased Ca2+ influx through MCP-1 in endothelial cells by monocyte adhesion

AU - Sakamoto, Takayuki

AU - Ishibashi, Toshiyuki

AU - Sakamoto, Nobuo

AU - Sugimoto, Koichi

AU - Egashira, Kensuke

AU - Ohkawara, Hiroshi

AU - Nagata, Kenji

AU - Yokoyama, Keiko

AU - Kamioka, Masashi

AU - Ichiki, Toshihiro

AU - Sugimoto, Naotoshi

AU - Kurabayashi, Masahiko

AU - Suzuki, Koji

AU - Takuwa, Yoh

AU - Maruyama, Yukio

PY - 2005/9/1

Y1 - 2005/9/1

N2 - Objective - Ca2+ plays an important role in tissue factor (TF) gene expression. We investigated the role of endogenous nitric oxide (NO) in the induction of TF expression in endothelial cells (ECs) by monocyte adhesion and the mechanisms of NO action. Methods and Results - Inhibition of endogenous NO by Nω-nitro-L-arginine methyl ester (L-NAME) enhanced TF promoter activity and protein expression induced in human coronary ECs by monocyte adhesion, as well as EC surface TF activity. L-NAME also induced monocyte chemoattractant protein-1 (MCP-1) expression, which was blocked by an NO donor, NOC18. Exogenous MCP-1 enhanced TF expression induced by monocyte adhesion, whereas adenovirus-mediated expression of the mutant MCP-1, 7ND, abolished the L-NAME enhancement of TF expression induced by monocyte adhesion. Monocyte attachment to L-NAME-treated ECs increased Ca2+ influx, which was prevented by NOC18, anti-MCP-1 antibody or 7ND. These results indicate that the binding of increased MCP-1 induced by endogenous NO blockade to CCR2 mediated the enhancement of Ca2+ influx only when monocytes adhered to ECs, which upregulated TF expression in ECs triggered by monocyte adhesion. Conclusion - MCP-1/CCR2 may play a role in Ca2+ influx-dependent TF regulation in the monocyte-EC interaction in the impairment of NO synthesis.

AB - Objective - Ca2+ plays an important role in tissue factor (TF) gene expression. We investigated the role of endogenous nitric oxide (NO) in the induction of TF expression in endothelial cells (ECs) by monocyte adhesion and the mechanisms of NO action. Methods and Results - Inhibition of endogenous NO by Nω-nitro-L-arginine methyl ester (L-NAME) enhanced TF promoter activity and protein expression induced in human coronary ECs by monocyte adhesion, as well as EC surface TF activity. L-NAME also induced monocyte chemoattractant protein-1 (MCP-1) expression, which was blocked by an NO donor, NOC18. Exogenous MCP-1 enhanced TF expression induced by monocyte adhesion, whereas adenovirus-mediated expression of the mutant MCP-1, 7ND, abolished the L-NAME enhancement of TF expression induced by monocyte adhesion. Monocyte attachment to L-NAME-treated ECs increased Ca2+ influx, which was prevented by NOC18, anti-MCP-1 antibody or 7ND. These results indicate that the binding of increased MCP-1 induced by endogenous NO blockade to CCR2 mediated the enhancement of Ca2+ influx only when monocytes adhered to ECs, which upregulated TF expression in ECs triggered by monocyte adhesion. Conclusion - MCP-1/CCR2 may play a role in Ca2+ influx-dependent TF regulation in the monocyte-EC interaction in the impairment of NO synthesis.

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