2005 Fiscal Year Final Research Report Summary
Molecular mechanism of inhibition of cell motility
| Project/Area Number |
16590163
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Kanazawa University Graduate School of Medicine |
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Principal Investigator |
SUGIMOTO Naotoshi Kanazawa University Graduate School of Medicine, Department of Vascular Molecular Physiology, Assistant Professor, 医学系研究科, 講師 (80272954)
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| Project Period (FY) |
2004 – 2005
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| Keywords | sphingosine-1-phosphate / cell migration / signal transduction / small G protein |
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| Research Abstract |
Sphingosine-1-phosphate (S1P) is a bioactive lysophospholipid that induces a variety of biological responses in diverse cell types. Many of these responses are mediated by S1P receptors, S1P_1/EDG1, S1P_3/EDG3, and S1P_2/EDG5. We previously showed that S1P_2/EDG5, via G_<12> and G_<13> proteins, mediated inhibiton of insulin-like growth factor-I (IGF-I)-induced Rac activation and cell migration, whereas S1P_1/EDG1 and S1P_3/EDG3 each alone, via G_1 protein, mediated Rac activation and stimulation of cell migration. However, it is not known how G_<12> and G_<13> proteins mediate inhibition of Rac and cell migration in S1P_2/EDG5 signaling. We found that the pretreatment with C3 toxin, which inactivates Rho, and the expresson of dominat negative Rho A prevented S1P_2/EDG5-mediated inhibition of Rac and cell migration. On other hand, the expression of constitutively active Rho inhibited IGF-I induced Rac activation and cell migration. However, Rho kinase inhibitors did not affect S1P_2/EDG5-mediated inhibition of Rac or cell migration. These results indicate that Rho, but not Rho kinase, mediates inhibition of Rac activity and cell mobility on stimulation of S1P_2/EDG5.
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[Journal Article] Endogenous NO blockade enhances tissue factor expression via increased Ca2+ influx through MCP-1 in endothelial cells by monocyte adhesion.2005
Author(s)
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.
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Journal Title
Arterioscler.Thromb.Vasc.Biol. 25(9)
Pages: 2005-2011
Description
「研究成果報告書概要(和文)」より
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[Journal Article] Thrombin-induced rapid geranylgeranylation of RhoA as an essential process for RhoA activation in endothelial cells.2005
Author(s)
Ohkawara H, Ishibashi T, Sakamoto T, Sugimoto K, Nagata K, Yokoyama K, Sakamoto N, Kamioka M, Matsuoka I, Fukuhara S, Sugimoto N, Takuwa Y, Maruyama Y.
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Journal Title
J Biol Chem. 280(11)
Pages: 10182-10188
Description
「研究成果報告書概要(和文)」より
-
-
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[Journal Article] Thrombin-induced rapid geranylgeranylation of RhoA as an essential process for RhoA activation in endothelial cells.2005
Author(s)
Ohkawara H., Ishibashi T., Sakamoto T., Sugimoto K., Nagata K., Yokoyama K., Sakamoto N., Kamioka M., Matsuoka I., Fukuhar S., Sugimoto N., Takuwa Y., Maruyama Y.
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Journal Title
J.Biol.Chem. 280(11)
Pages: 10182-10188
Description
「研究成果報告書概要(欧文)」より
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[Journal Article] Endogenous NO blockade enhances tissue facto expression via increased Ca2+ influx through MCP-1 in endothelial cells by monocyte adhesion.2005
Author(s)
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.
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Journal Title
Arterioscler.Thromb.Vasc.Biol. 25(9)
Pages: 2005-2011
Description
「研究成果報告書概要(欧文)」より
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