| Project/Area Number |
11670602
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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 |
Respiratory organ internal medicine
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| Research Institution | Fukuoka University |
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Principal Investigator |
WATANABA Kentaro School of Medicine, Fukuoka University Lecturer, 医学部, 講師 (80158625)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIDA Minoru School of Medicine, Fukuoka University Professor, 医学部, 教授 (60078772)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | human pulmonary artery smooty muscle cells / prostacyclin (pg12) / nitric oxide (NO, nitrogen monooxide) / cytokines / LIPOPOLYSACCHARIDE (LPS) / COX-2s / NO合成酵素 / 血管内細胞 / プロスタグランディン / 肺動脈平滑筋細胞 / Nitric oxide(NO) / Prostacyclin(PGI_2) / NO合成酵素(NOS) |
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| Research Abstract |
Human pulmonary artery smooth muscle cells (HPASMC) were isolated and cultured from autopsy materials, and the effect of sodium nitroprusside (SNP) on cytokine- or lipopolysaccharide (LPS)-induced PGI2 production and expression of COX-2 antigen by HPASMC were examined to elucidate the relationship of the production of NO and prostaglandins by HPASMC. Eicosanoid profile by LPS-stimulated human umbilical vein endothelial ceUs(HUVEC) was also examined by HPLC.
1) The enhanced production of PGI2 by LPS- and IL-1β-treated HPASMC was further augmented when HPASMC were treated with LPS or EL-1βtogether with SNP.
2) In HUVEC, LPS enhanced the production of cyclooxygenase derivatives, but did not clearly enhance the production of lipoxygenase products. In contrasts, LPS enhanced the production of both cyclooxygenae and lipoxygenase products in HPASMC.
3) Western blot analysis revealed that IL-1βaugmented the expression of COX-2 protein in HPASMC,
From these experimental findings, it is suggested that
1) NO enhances PGI2 production by HPASMC through the increased expression of COX-2 antigen.
2) Pulmonary artery smooth muscle cells as well as endothelial cells could actively participate in the regulation of pulmonary blood flow and tonus of pulmonary artery by the interaction of NO and prostaglandins.
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