Project/Area Number |
10671772
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
病態科学系歯学(含放射線系歯学)
|
Research Institution | Kagoshima University |
Principal Investigator |
NOIKURA Takenori Kagoshima University, Faculty of Dentistry, Professor, 歯学部, 教授 (40102561)
|
Co-Investigator(Kenkyū-buntansha) |
MARUYAMA Ikuro Kagoshima University, Faculty of Medicine, Professor, 医学部, 教授 (20082282)
|
Project Period (FY) |
1998 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1998: ¥1,800,000 (Direct Cost: ¥1,800,000)
|
Keywords | Adverse reaction / Late phase / Endothelial cells / P-selectin / NF-kappa B / nitruc oxide / iNOS / Contrast media / P-selectin、ICAM-1 / NF-κBの活性化 / 誘導型NO合成酵素(iNOS) / NOの生産 / P-selectin,ICAM-1 / 誘導型NO合成酵素(NOS) / NOの産生 |
Research Abstract |
Endothelial Selectins, such as P-selectin and E-selectin, mediate cell adhesion of monocytes or neutrophils to activated endothelial cells. Previously we reported an upregulated expression of inflammatory cytokines by P-selectin-mediated neutrophil attachment to activated endothelium stimulated by contrast media. We examined the effect of endothelial selectins on the expression of inflammatory cytokines, nitric oxide production and on the activation of NF-kappa B. We found that the soluble forms of P-selectin and E-selectin as well as the monocyte-endothelial interaction induced upregulated the expression of inflammatory cytokines and the production of nitric oxide. These expression of inflammatory cytokines involved the activation of NF-kappa B pathway by the reactive oxygen intermediate (ROI). P-selectin specifically induced β2-integrin (CD11b)-mediated sticky adhesion of monocytes, via ROI generation. Then P-selectin-mediated rapid activation of NF-kappa B, which was augmented by following with β2-integrin (CD11b)-induced sticky adhesion. The binding of endothelial selectins to monocytes in the area of vascular activation by contrast media is considered to be a component of the mechanism that initiates thrombosis and hypotension after the administration of contrast media.
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