| ○種別 (必須): | □ | 学術論文 (審査論文)
| [継承] |
| ○言語 (必須): | □ | 英語
| [継承] |
| ○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. | 岩田 武男
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 2. | 桒島 正道
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 3. | 助野 晃子 ([徳島大学.大学院ヘルスバイオサイエンス研究部.学長裁量プロジェクト]/->個人[原田 晃子])
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 4. | 石丸 直澄 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.口腔分子病態学])
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 5. | 林 良夫
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 6. | (英) Wabitsch Martin (日) (読)
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 7. | 水澤 典子 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.基礎歯学系.口腔生命科学])
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 8. | 板倉 光夫
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 9. | 吉本 勝彦
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| ○題名 (必須): | □ | (英) YKL-40 secreted from adipose tissue inhibits degradation of type I collagen. (日)
| [継承] |
| ○副題 (任意): |
| ○要約 (任意): | □ | (英) Obesity is considered a chronic low-grade inflammatory status and the stromal vascular fraction (SVF) cells of adipose tissue (AT) are considered a source of inflammation-related molecules. We identified YKL-40 as a major protein secreted from SVF cells in human visceral AT. YKL-40 expression levels in SVF cells from visceral AT were higher than in those from subcutaneous AT. Immunofluorescence staining revealed that YKL-40 was exclusively expressed in macrophages among SVF cells. YKL-40 purified from SVF cells inhibited the degradation of type I collagen, a major extracellular matrix of AT, by matrix metalloproteinase (MMP)-1 and increased rate of fibril formation of type I collagen. The expression of MMP-1 in preadipocytes and macrophages was enhanced by interaction between these cells. These results suggest that macrophage/preadipocyte interaction enhances degradation of type I collagen in AT, meanwhile, YKL-40 secreted from macrophages infiltrating into AT inhibits the type I collagen degradation. (日)
| [継承] |
| ○キーワード (推奨): | 1. | (英) Adipocytes (日) (読)
| [継承] |
| 2. | (英) Adipose Tissue (日) (読)
| [継承] |
| 3. | (英) Adult (日) (読)
| [継承] |
| 4. | (英) Aged (日) (読)
| [継承] |
| 5. | (英) Cells, Cultured (日) (読)
| [継承] |
| 6. | (英) Coculture Techniques (日) (読)
| [継承] |
| 7. | (英) Collagen Type I (日) (読)
| [継承] |
| 8. | (英) Female (日) (読)
| [継承] |
| 9. | (英) Glycoproteins (日) (読)
| [継承] |
| 10. | (英) Humans (日) (読)
| [継承] |
| 11. | (英) Inflammation (日) (読)
| [継承] |
| 12. | (英) Lectins (日) (読)
| [継承] |
| 13. | (英) Macrophages (日) (読)
| [継承] |
| 14. | (英) Male (日) (読)
| [継承] |
| 15. | (英) Matrix Metalloproteinase 1 (日) (読)
| [継承] |
| 16. | (英) Middle Aged (日) (読)
| [継承] |
| 17. | (英) Obesity (日) (読)
| [継承] |
| 18. | (英) Stromal Cells (日) (読)
| [継承] |
| ○発行所 (推奨): |
| ○誌名 (必須): | □ | Biochemical and Biophysical Research Communications ([Elsevier])
(pISSN: 0006-291X, eISSN: 1090-2104)
| ○ISSN (任意): | □ | 1090-2104
ISSN: 0006-291X
(pISSN: 0006-291X, eISSN: 1090-2104) Title: Biochemical and biophysical research communicationsTitle(ISO): Biochem Biophys Res CommunPublisher: Elsevier Inc. (NLM Catalog)
(Scopus)
(CrossRef)
(Scopus information is found. [need login]) | [継承] |
| [継承] |
| ○巻 (必須): | □ | 388
| [継承] |
| ○号 (必須): | □ | 3
| [継承] |
| ○頁 (必須): | □ | 511 516
| [継承] |
| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2009年 8月 8日 (平成 21年 8月 8日)
| [継承] |
| ○URL (任意): |
| ○DOI (任意): | □ | 10.1016/j.bbrc.2009.08.024 (→Scopusで検索)
| [継承] |
| ○PMID (任意): | □ | 19666003 (→Scopusで検索)
| [継承] |
| ○CRID (任意): |
| ○WOS (任意): |
| ○Scopus (任意): |
| ○機関リポジトリ : | □ | 109641
| [継承] |
| ○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 Medical Pharmacology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima 770-8504, Japan. (日)
| [継承] |
| 2. | (英) PublicationType: Journal Article (日)
| [継承] |
| 3. | (英) PublicationType: Research Support, Non-U.S. Gov't (日)
| [継承] |