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<Review> Bone anabolic action of parathyroid hormone
https://kindai.repo.nii.ac.jp/records/10583
https://kindai.repo.nii.ac.jp/records/10583af4c5197-62fe-4701-988a-7a4cc412e4de
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
AA0050842X-20121200-0057.pdf (7.7 MB)
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| Item type | ☆一般雑誌記事 / Article(1) | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|
| 公開日 | 2015-02-04 | |||||||||
| タイトル | ||||||||||
| タイトル | <Review> Bone anabolic action of parathyroid hormone | |||||||||
| 言語 | en | |||||||||
| 著者 |
Kaji, Hiroshi
× Kaji, Hiroshi
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| 言語 | ||||||||||
| 言語 | eng | |||||||||
| キーワード | ||||||||||
| 主題 | parathyroid hormone, bone, osteoblast, smad, β-catenin | |||||||||
| 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 | article | |||||||||
| 著者 所属 | ||||||||||
| 値 | Department of Physiology and Regenerative Medicine, Kinki University Faculty of Medicine | |||||||||
| 著者所属(翻訳) | ||||||||||
| 値 | Kinki University | |||||||||
| 版 | ||||||||||
| 出版タイプ | VoR | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||
| 出版者 名前 | ||||||||||
| 出版者 | Kinki University Medical Association | |||||||||
| 書誌情報 |
en : ACTA MEDICA KINKI UNIVERSITY 巻 37, 号 2, p. 57-62, 発行日 2012-12-01 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | ISSN | |||||||||
| 収録物識別子 | 03866092 | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | [Abstract] Parathyroid hormone (PTH) is a potent bone-forming agent that increases bone mineral density and reduces fracture risk in osteoporotic patients. Although several studies suggest that the anabolic action of PTH is exerted partly through local growth factors and transcriptional regulators as well as by anti-apoptotic action in osteoblasts, the precise mechanisms by which PTH exerts its anabolic action on bone are incompletely understood. We demonstrated that PTH rapidly increases the level of Smad3, and that PTH-Smad3 signal is involved in antiapoptotic effects in osteoblasts. Moreover, PTH stimulated osteoblast β-catenin levels via Smad3 in osteoblastic cells. Our further study indicated that PTH induces osteoblast β- catenin levels via Smad3 independently of, and dependently on, TGF-β in the early and late induction phases, respectively. In addition, we previously showed that inhibition of ERK1/2 enhanced Smad3-induced bone anabolic action in osteoblasts. These findings suggested that changes in gene expression associated with the altered Smad3-induced signal brought about by an ERK1/2 inhibitor might identify novel bone anabolic factors in osteoblasts. We therefore performed a comparative DNA microarray analysis between empty vector-transfected mouse osteoblastic MC3T3-E1 cells and ERK1/2 inhibitor-treated stable Smad3-overexpressing MC3T3-E1 cells. Among the novel factors, Tmem119 was selected on the basis of its rapid induction by PTH independent of later increases in endogenous TGF-β. Tmem119 seemed to be an important osteoblast differentiation factor in the pathway downstream of PTH and Smad3 signal in osteoblasts. | |||||||||
| 資源タイプ | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | Article | |||||||||
| フォーマット | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | application/pdf | |||||||||
