PMID- 16020745
OWN - NLM
STAT- MEDLINE
DCOM- 20060106
LR  - 20131121
IS  - 1524-4636 (Electronic)
IS  - 1079-5642 (Linking)
VI  - 25
IP  - 9
DP  - 2005 Sep
TI  - Endogenous NO blockade enhances tissue factor expression via increased Ca2+ 
      influx through MCP-1 in endothelial cells by monocyte adhesion.
PG  - 2005-11
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 
      Nomega-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. CONCLUSIONS: MCP-1/CCR2 may play a role in Ca2+ 
      influx-dependent TF regulation in the monocyte-EC interaction in the impairment 
      of NO synthesis.
FAU - Sakamoto, Takayuki
AU  - Sakamoto T
AD  - First Department of Internal Medicine, Fukushima Medical University, 1 
      Hikarigaoka, Fukushima, 960-1295, Japan.
FAU - Ishibashi, Toshiyuki
AU  - Ishibashi T
FAU - Sakamoto, Nobuo
AU  - Sakamoto N
FAU - Sugimoto, Koichi
AU  - Sugimoto K
FAU - Egashira, Kensuke
AU  - Egashira K
FAU - Ohkawara, Hiroshi
AU  - Ohkawara H
FAU - Nagata, Kenji
AU  - Nagata K
FAU - Yokoyama, Keiko
AU  - Yokoyama K
FAU - Kamioka, Masashi
AU  - Kamioka M
FAU - Ichiki, Toshihiro
AU  - Ichiki T
FAU - Sugimoto, Naotoshi
AU  - Sugimoto N
FAU - Kurabayashi, Masahiko
AU  - Kurabayashi M
FAU - Suzuki, Koji
AU  - Suzuki K
FAU - Takuwa, Yoh
AU  - Takuwa Y
FAU - Maruyama, Yukio
AU  - Maruyama Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20050714
PL  - United States
TA  - Arterioscler Thromb Vasc Biol
JT  - Arteriosclerosis, thrombosis, and vascular biology
JID - 9505803
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Enzyme Inhibitors)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 9035-58-9 (Thromboplastin)
RN  - SY7Q814VUP (Calcium)
RN  - V55S2QJN2X (NG-Nitroarginine Methyl Ester)
SB  - IM
MH  - Calcium/metabolism
MH  - Calcium Signaling/physiology
MH  - Cell Adhesion/drug effects/immunology
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Coronary Vessels/cytology
MH  - Endothelium, Vascular/cytology/immunology/*metabolism
MH  - Enzyme Inhibitors/pharmacology
MH  - Gene Transfer Techniques
MH  - Humans
MH  - Monocytes/*cytology/immunology
MH  - NG-Nitroarginine Methyl Ester/pharmacology
MH  - Nitric Oxide/antagonists & inhibitors/*metabolism
MH  - Thromboplastin/*metabolism
EDAT- 2005/07/16 09:00
MHDA- 2006/01/07 09:00
CRDT- 2005/07/16 09:00
PHST- 2005/07/16 09:00 [pubmed]
PHST- 2006/01/07 09:00 [medline]
PHST- 2005/07/16 09:00 [entrez]
AID - 01.ATV.0000178171.61754.cd [pii]
AID - 10.1161/01.ATV.0000178171.61754.cd [doi]
PST - ppublish
SO  - Arterioscler Thromb Vasc Biol. 2005 Sep;25(9):2005-11. doi: 
      10.1161/01.ATV.0000178171.61754.cd. Epub 2005 Jul 14.