○種別 (必須): | □ | 学術論文 (審査論文)
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○言語 (必須): | □ | 英語
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○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. | 香美 祥二 ([徳島大学])
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| 2. | 漆原 真樹 ([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.内科系.小児科学]/[徳島大学.病院.診療科.小児·周産·女性科.小児科])
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| 3. | 近藤 秀治
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| 4. | (英) Toshihiko Hayashi (日) (読)
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| 5. | (英) Yamano Hiroko (日) (読)
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| 6. | (英) Kiemens Loster (日) (読)
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| 7. | (英) Dorte Vossmeyer (日) (読)
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| 8. | (英) Werner Reutter (日) (読)
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| 9. | 黒田 𣳾弘
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○題名 (必須): | □ | (英) Effects of Anti-α1 Integrin Subunit Antibody on Anti-Thy-1 Glomerulonephritis (日)
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○副題 (任意): |
○要約 (任意): | □ | (英) alpha1beta1 integrin is a potential collagen-binding extracellular matrix receptor that mediates collagen-dependent cell adhesion, proliferation, migration, and collagen matrix assembly and thereby may participate in the wound healing and pathologic scarring observed in some damaged organs. To clarify the role of alpha1beta1 integrin predominantly expressed on the mesangial cell (MC) surface in nephritic glomeruli, we investigated the involvement of MC-alpha1beta1 integrin in rat anti-Thy-1 glomerulonephritis (GN) by administering function-blocking monoclonal mouse anti-rat alpha1 integrin subunit antibody (anti-alpha1 Ab). Assay of collagen types I and IV mixed gel contraction, an in vitro model of pathologic collagen matrix remodeling, with function-blocking anti-alpha1 Ab and anti-beta1 Ab, revealed that collagen I and IV matrix reorganization is mediated by MC-alpha1beta1 integrin. In addition, conditioned medium from isolated Day 3 anti-Thy-1 nephritic glomeruli showed increased activity of MC-alpha1beta1 integrin-induced mixed collagen gel contraction as compared with that from isolated normal rat glomeruli. Treatment of Day 3 conditioned medium with anti-platelet-derived growth factor-BB antibody significantly inhibited conditioned media-induced gel contraction, whereas treatment with anti-transforming growth factor-beta antibody did not have a significant effect. Rats that received anti-alpha1 Ab from the left renal artery 3 days after anti-Thy-1 GN induction showed significant decreases of glomerular hypercellularity and mesangial matrix accumulation, including collagen I and IV in the left kidney, compared with those rats in which the left kidney received control mouse IgG1. These results suggest that MC-alpha1beta1 integrin is an important extracellular matrix receptor mediating mesangial remodeling characterized by MC proliferation and mesangial matrix reorganization in anti-Thy-1 GN. Platelet-derived growth factor-BB may be involved in early collagen matrix reorganization leading to pathologic mesangial remodeling in this GN model. (日)
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○キーワード (推奨): | 1. | (英) Animals (日) (読)
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| 2. | (英) Antibodies, Monoclonal (日) (読)
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| 3. | (英) Antigens, Thy-1 (日) (読)
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| 4. | コラーゲン (collagen)
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| 5. | 細胞外マトリックス (extracellular matrix)
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| 6. | (英) Glomerular Mesangium (日) (読)
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| 7. | (英) Glomerulonephritis (日) (読)
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| 8. | (英) Integrin alpha1beta1 (日) (読)
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| 9. | (英) Integrins (日) (読)
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| 10. | (英) Male (日) (読)
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| 11. | (英) Platelet-Derived Growth Factor (日) (読)
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| 12. | (英) Rats (日) (読)
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| 13. | (英) Rats, Sprague-Dawley (日) (読)
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| 14. | (英) Transforming Growth Factor beta (日) (読)
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| 15. | (英) Wound Healing (日) (読)
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○発行所 (推奨): |
○誌名 (必須): | □ | Laboratory Investigation; a Journal of Technical Methods and Pathology (United States and Canadian Academy of Pathology)
(pISSN: 0023-6837, eISSN: 1530-0307)
○ISSN (任意): | □ | 0023-6837
ISSN: 0023-6837
(pISSN: 0023-6837, eISSN: 1530-0307) Title: Laboratory investigation; a journal of technical methods and pathologyTitle(ISO): Lab InvestPublisher: Springer Nature (NLM Catalog)
(Scopus)
(CrossRef)
(Scopus information is found. [need login])
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○巻 (必須): | □ | 82
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○号 (必須): | □ | 9
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○頁 (必須): | □ | 1219 1227
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○都市 (任意): |
○年月日 (必須): | □ | 西暦 2002年 9月 初日 (平成 14年 9月 初日)
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○URL (任意): |
○DOI (任意): | □ | 10.1097/01.LAB.0000027835.77351.BF (→Scopusで検索)
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○PMID (任意): | □ | 12218083 (→Scopusで検索)
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○CRID (任意): |
○WOS (任意): |
○Scopus (任意): | □ | 2-s2.0-0036707503
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○備考 (任意): | 1. | (英) Article.PublicationTypeList.PublicationType: Journal Article (日)
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| 2. | (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't (日)
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