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

Research output: Contribution to journalArticle

26 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)2005-2011
Number of pages7
JournalArteriosclerosis, thrombosis, and vascular biology
Volume25
Issue number9
DOIs
Publication statusPublished - Sep 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

Cite this

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.

In: Arteriosclerosis, thrombosis, and vascular biology, Vol. 25, No. 9, 01.09.2005, p. 2005-2011.

Research output: Contribution to journalArticle

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, vol. 25, no. 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. In: Arteriosclerosis, thrombosis, and vascular biology. 2005 ; Vol. 25, No. 9. pp. 2005-2011.
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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

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