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著作: [漆原 真樹]/Ohashi Naro/Miyata Kayoko/Satou Ryousuke/Acres Omar W/Kobori Hiroyuki/Addition of angiotensin II type 1 receptor blocker to CCR2 antagonist markedly attenuates crescentic glomerulonephritis./[Hypertension]

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EID
243435
EOID
660985
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0
LastModified
2012年9月19日(水) 13:59:14
Operator
三木 ちひろ
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TRUE
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Owner
漆原 真樹
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種別 必須 学術論文(審査論文)
言語 必須 英語
招待 推奨
審査 推奨
カテゴリ 推奨
共著種別 推奨
学究種別 推奨
組織 推奨
著者 必須
  1. 漆原 真樹([徳島大学.病院.診療科.小児·周産·女性科.小児科])
    役割 任意
    貢献度 任意
    学籍番号 推奨
  2. (英) Ohashi Naro
    役割 任意
    貢献度 任意
    学籍番号 推奨
  3. (英) Miyata Kayoko
    役割 任意
    貢献度 任意
    学籍番号 推奨
  4. (英) Satou Ryousuke
    役割 任意
    貢献度 任意
    学籍番号 推奨
  5. (英) Acres Omar W
    役割 任意
    貢献度 任意
    学籍番号 推奨
  6. (英) Kobori Hiroyuki
    役割 任意
    貢献度 任意
    学籍番号 推奨
題名 必須

(英) Addition of angiotensin II type 1 receptor blocker to CCR2 antagonist markedly attenuates crescentic glomerulonephritis.

副題 任意
要約 任意

(英) The monocyte chemoattractant protein-1 (MCP-1)/CC-chemokine receptor 2 (CCR2) pathway plays a critical role in the development of antiglomerular basement membrane (anti-GBM) nephritis. We recently showed angiotensin II (Ang II) infusion in rats activated MCP-1 and transforming growth factor-1 (TGF-1), which in turn induced macrophage infiltration of renal tissues. This study was performed to demonstrate that combination therapy with a CCR2 antagonist (CA) and an Ang II type 1 receptor blocker (ARB) ameliorated renal injury in the anti-GBM nephritis model. An anti-GBM nephritis rat model developed progressive proteinuria and glomerular crescent formation, accompanied by increased macrophage infiltration and glomerular expression of MCP-1, angiotensinogen, Ang II, and TGF-1. Treatment with CA alone or ARB alone moderately ameliorated kidney injury; however, the combination treatment with CA and ARB dramatically prevented proteinuria and markedly reduced glomerular crescent formation. The combination treatment also suppressed the induction of macrophage infiltration, MCP-1, angiotensinogen, Ang II, and TGF-1 and reversed the fibrotic change in the glomeruli. Next, primary cultured glomerular mesangial cells (MCs) stimulated by Ang II showed significant increases in MCP-1 and TGF-1 expression. Furthermore, cocultured model consisting of MCs, parietal epithelial cells, and macrophages showed an increase in Ang II-induced cell proliferation and collagen secretion. ARB treatment attenuated these augmentations. These data suggest that Ang II enhances glomerular crescent formation of anti-GBM nephritis. Moreover, our results demonstrate that inhibition of the MCP-1/CCR2 pathway with a combination of ARB effectively reduces renal injury in anti-GBM nephritis.

キーワード 推奨
  1. 分散分析(analysis of variance)
  2. (英) Angiotensin II
  3. (英) Angiotensin II Type 1 Receptor Blockers
  4. (英) Animals
  5. (英) Anti-Glomerular Basement Membrane Disease
  6. 血圧(blood pressure)
  7. (英) Cell Proliferation
  8. (英) Chemokine CCL2
  9. (英) Disease Models, Animal
  10. (英) Enzyme-Linked Immunosorbent Assay
  11. 免疫組織化学(immunohistochemistry)
  12. (英) Kidney
  13. (英) Macrophages
  14. (英) Male
  15. (英) Rats
  16. (英) Rats, Inbred WKY
  17. (英) Receptors, CCR2
  18. レニン·アンジオテンシンシステム(Renin-angiotensin System)
  19. (英) Reverse Transcriptase Polymerase Chain Reaction
  20. (英) Transforming Growth Factor beta1
発行所 推奨
誌名 必須 Hypertension([American Heart Association])
(pISSN: 0194-911X, eISSN: 1524-4563)
ISSN 任意 1524-4563
ISSN: 0194-911X (pISSN: 0194-911X, eISSN: 1524-4563)
Title: Hypertension (Dallas, Tex. : 1979)
Title(ISO): Hypertension
Publisher: American Heart Association
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
必須 57
必須 3
必須 586 593
都市 任意
年月日 必須 2011年 1月 31日
URL 任意
DOI 任意 10.1161/HYPERTENSIONAHA.110.165704    (→Scopusで検索)
PMID 任意 21282555    (→Scopusで検索)
NAID 任意
WOS 任意
Scopus 任意
評価値 任意
被引用数 任意
指導教員 推奨
備考 任意
  1. (英) Affiliation: Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, LA 70112-2699, USA.

  2. (英) PublicationType: Journal Article

  3. (英) PublicationType: Research Support, N.I.H., Extramural