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ウサギ関節軟骨細胞のケラタン硫酸代謝におけるtransforming growth factor-betaの役割
https://kindai.repo.nii.ac.jp/records/2002205
https://kindai.repo.nii.ac.jp/records/200220536e7b0b9-c894-4307-98e3-47ffe6dc5365
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
AN00063584-19930625-0241.pdf (706.7 KB)
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| アイテムタイプ | ☆紀要論文 / Departmental Bulletin Paper(1) | |||||||||
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| 公開日 | 2024-12-20 | |||||||||
| タイトル | ||||||||||
| タイトル | ウサギ関節軟骨細胞のケラタン硫酸代謝におけるtransforming growth factor-betaの役割 | |||||||||
| 言語 | ja | |||||||||
| タイトル | ||||||||||
| タイトル | The role of transforming growth factor-beta in keratan sulfate metabolism in rabbit articular chondrocytes | |||||||||
| 言語 | en | |||||||||
| 著者 |
大谷, 和裕
× 大谷, 和裕
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| 言語 | ||||||||||
| 言語 | jpn | |||||||||
| キーワード | ||||||||||
| 主題 | articular cartilage, keratan sulfate, cytokine, growth factor, transforming growth factor beta (TGF-β) | |||||||||
| 資源タイプ | ||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||
| 資源タイプ | departmental bulletin paper | |||||||||
| 出版タイプ | ||||||||||
| 出版タイプ | AM | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||
| 出版者 名前 | ||||||||||
| 出版者 | 近畿大学医学会 | |||||||||
| 言語 | ja | |||||||||
| bibliographic_information |
ja : 近畿大学医学雑誌 en : Medical Journal of Kinki University 巻 18, 号 2, p. 241-252, 発行日 1993-06-25 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | PISSN | |||||||||
| 収録物識別子 | 03858367 | |||||||||
| 内容記述 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | Keratan sulfate is the specific molecule in glycosaminoglycan, which is the matrix of articular cartilage, and is produced by chondrocytes. There is evidence that levels of serum keratan sulfate might reflect turnover of articular cartilage in vivo. To gain more insight into related events, the effects of cytokines and growth factors (interleukin-1, interleukin-6, tumor necrosis factor alfa, transforming growth factor beta (TGF-β), platelet derived growth factor, and insulin like growth factor) on keratan sulfate release in vitro were investigated. All cytokines inhibited keratan sulfate release, whereas growth factors stimulated keratan sulfate release. TGF-β exhibited the most striking effect on keratan sulfate release in the chondrocytes and, this effect was receptor mediated since pretreatment with TGF-β reduced the effect (down-regulation). Actionomycin D and cycloheximide completely blocked the TGF-β mediated keratan sulfate increase. TGF-β enhanced the expression of core protein mRNA. Thus, TGF-β probably enhances keratan sulfate through de novo synthesis. Cytokines and growth factors do appear to regulate keratan sulfate release. With its effects on synthesis of matrix proteins, TGF-β may promote repair in diseased articular cartilage. Moreover, our study indicates that the levels of keratan sulfate in the blood of healthy subjects and in subjects with disease (rheumatoid arthritis, rapidly destructive coxarthropathy and osteoarthritis) may reflect turnover of articular cartilage. | |||||||||
| 言語 | en | |||||||||
| 内容記述 | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | 本文データはCiNiiから複製したものである。 | |||||||||
| 言語 | ja | |||||||||
