| Project/Area Number |
11671523
|
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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 |
Anesthesiology/Resuscitation studies
|
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| Research Institution | Hyogo College of Medicine (2000)
Teikyo University (1999) |
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Principal Investigator |
ONO Yukari Hyogo College of Medicine. Research Associate, 医学部, 助手 (30312002)
|
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| Co-Investigator(Kenkyū-buntansha) |
OKADA Kazuo Teikyo Univ. School of Medicine. professor, 医学部, 教授 (30082093)
TASHIRO Chikara Hyogo College of Medicine. professor, 医学部, 教授 (20107048)
KANGAWA Kenji National Cardiovascular Center., 研究所, 部長 (00112417)
中村 到 帝京大学, 医学部, 助手 (50307196)
|
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| Project Period (FY) |
1999 – 2000
|
| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 2000: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1999: ¥3,100,000 (Direct Cost: ¥3,100,000)
|
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| Keywords | adrenomedullin / sepsis / lipopolysaccharide / thymus / receptor / エンドトキシン / CRLR / RAMPs / 肺 |
|---|
| Research Abstract |
Plasma concentrations of adrenomedullin (AM) are markedly increased during sepsis, but the role of AM has not been clarified. Coexpression of calcitonin receptor-like receptor (CRLR) and receptor activity modifying protein (RAMP) 2 or 3 have been reported to form the adrenomedullin (AM) specific receptor. We examined the expression of CRLR and RAMP1, 2, and 3 in several tissues from mice in a sepsis model induced by lipopolysaccharide (LPS). High expression of CRLR and RAMP2 mRNA was observed in lungs of normal mice, but it was markedly decreased in endotoxemic mice. It is suggested that the abundant binding sites of AM in lungs are formed by CRLR and RAMP2 in healthy subjects and that their reduction should contribute to the increase of plasma AM concentrations during sepsis. In contrast, LPS treatment markedly increased RAMP3 gene expression in lungs, spleen, and thymus. It is revealed that the distributions of receptor or binding sites of AM are changed in sepsis, and it is suggested that AM plays distinct roles in the clinical course of this syndrome.
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