1998 Fiscal Year Final Research Report Summary
The role of nitric oxide in PGI_2 production by human pulmonary artery smooth muscle cells
| Project/Area Number |
09670636
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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 Fukuoka Univ., School of Med., Assist.Prof., 医学部, 講師 (80158625)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIDA Minoru Fukuoka Univ., School of Med., Professor, 医学部, 教授 (60078772)
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| Project Period (FY) |
1997 – 1998
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| Keywords | human pulmonary artery smooth muscle cells / prostacyclin(PGI_2) / nitric oxide(NO,nitrogen monooxide) / cytokines / lipopolysaccharide(LPS) / IL-6 |
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| Research Abstract |
Human pulmonary arlcry smooth musclc cclls(HPASMC) were isolated and culfured from autopsy materials, and the effect of nitric oxide(NO) on PG12 production by HPASMC was examined and the effect of IL-6 on NO production by HPASMC was also examined to elucidate the relationship of the production of NO and proslaglandins by H PASMC.
1)LPS, IL-1beta and TNF_2 enhanced the production of NO by HPASMC.
2)The enlhanced production of PGI_2 by LPS-and IL-1beta-treated HPASMC was further augmenter when HPASMC were treated with LPS or IL-1beta together with sodium nitroprusside.
3)The enhanced production of PGI_2 by LPS- and IL-1beta-treated HPASMC was attenuated when HPASMC were treated with LPS or IL-1beta together with L-NMMA.
4)Methylene blue(MeB) suppressed PGI_2 production by HPASM C, and attenuated the enhanced production of PGI_2 by HPASMC treated with LPS or IL-1beta.
5)Although IL-6 did not changed the basal production of NO by HPASMC, it attenuated the enhanced production of NO by HPASMC treated with LPS or IL-1beta.
6)LPS, IL-1beta, TNF_2 and SNP up to the maximum concentrations used in these experiments did not increase thc LDH release from HPASMC treated with these agents.
From these experimental lindings it is suggested that
(1)NO enhances PGI_2 production by human pulmonary arlery smooth muscle cells.
(2)IL-6 suppresses not only the production of prostagland ins but NO by human pulmonary artery smooth muscle cells. this result could show antiinllammatory aspect of IL-6 in vivo.
(3)Pulmonary artery smooth lb muscles could actively participate in the regulation of pumonary blood flow and tonus of pulmonary artery by the interaction of NO and prostaglandins.
Further examinations are needed to elucidate the. mechanisms of NO-mediated enhancement of PGl_2 production and IL-6-mediated suppression of NO production by examining the induction of COX-2 and iNOS proteins and genes.
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