| Project/Area Number |
07670686
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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 |
WATANABE Kentaro Second Department of Internal Medicine, School of Medicine, Fukuoka University Assistant Professor, 医学部, 講師 (80158625)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIDA Minoru Second Department of Internal Medicine, School of Medicine, Fukuoka University P, 医学部, 教授 (60078772)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1996: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1995: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | pulmonary artery smooth muscle cells / prostacyclin (PGI_2) / nitric oxide (NO,nitrogen monooxide) / cytokines / lipopolysaccharide (LPS) / NO donor / NO synthase inhibitor / プロスタサイクリン / NO / サイトカン / 一酸化窒素(NO) |
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| Research Abstract |
Human pulmonary artery smooth muscle cells (HAPSMC) were cultured from autopsy materials, and the effect of lipopolysaccharide (LPS) and cytokines on PGI_2 production and arachidonic acid metabolism by HPASMC was examined.
1) LPS,IL-1_<beta> and TNF_<alpha> enhanced the production of PGI_2 and nitric oxide (NO) by HPASMC.
2) HPLC analysis revealed that 10mug/ml of LPS and 200U/ml of IL-1_<beta> enhanced the production of both lipoxygenase (LO) and cyclooxygenase (COX) products, and 500U/ml of TNFalpha enhanced that of COX products.
3) IL-6 suppressed the basal production of PGI_2 by HPASMC,and attenuated the enhancement of PGI_2 production by HPASMC treated with LPS,IL-1_<beta> or TNF_<alpha>.
4) The enhancement of PGI_2 production by LPS and IL-1_<beta> was attenuated when HPASMC were treated with LPS or IL-1_<beta> together with L-NMMA,NO synthase inhibitor.
5) The enhancement of PGI_2 production by LPS and IL-1_<beta> was augmented when HPASMC were treated with LPS or IL-1_<beta> together with sodium nitroprusside, NO donor.
6) From these experimental findings, it is suggested that
(1) Human pulmonary artery smooth muscle cells could produce NO and PGI_2 in response to LPS or cytokines.
(2) NO could enhance the production of PGI_2 by pulmonary artery smooth muscle cells
(3) Pulmonary srtery smooth muscles could actively participate in the regulation of pulmonary blood flow and tonus of pulmonary artery by producing NO and PGI_2.
Further examination is needed to elucidate the mechanism of the enhancement of PGI_2 production by NO.
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