『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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EID=268578EID:268578, Map:0, LastModified:2013年8月19日(月) 20:56:00, Operator:[遠藤 逸朗], Avail:TRUE, Censor:0, Owner:[遠藤 逸朗], Read:継承, Write:継承, Delete:継承.
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): Peer Review [継承]
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. (英) Kuriwaka-Kido Rika (日) (読)
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[継承]
2. (英) Kido Shinsuke (日) (読)
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[継承]
3. (英) Miyatani Yuka (日) (読)
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[継承]
4. (英) Ito Yuji (日) (読)
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[継承]
5.近藤 剛史
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[継承]
6. (英) Omatsu Takashi (日) (読)
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学籍番号 (推奨):
[継承]
7. (英) Dong Bingzi (日) (読)
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[継承]
8.遠藤 逸朗 ([徳島大学.大学院医歯薬学研究部.保健科学域.保健科学部門.医用検査学系.生体機能解析学])
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[継承]
9.宮本 賢一 ([徳島大学.大学院医歯薬学研究部.医学域.栄養科学部門.医科栄養学系.応用栄養学])
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10.松本 俊夫
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[継承]
題名 (必須): (英) Parathyroid hormone (1-34) counteracts the suppression of interleukin-11 expression by glucocorticoid in murine osteoblasts: a possible mechanism for stimulating osteoblast differentiation against glucocorticoid excess.  (日)    [継承]
副題 (任意):
要約 (任意): (英) Glucocorticoid (GC) excess causes a rapid loss of bone with a reduction in bone formation. Intermittent PTH (1-34) administration stimulates bone formation and counteracts the inhibition of bone formation by GC excess. We have previously demonstrated that mechanical strain enhances interleukin (IL)-11 gene transcription by a rapid induction of FosB expression and protein kinase C (PKC)--mediated phosphorylation of phosphorylated mothers against decapentaplegic (Smad)-1. Because IL-11 suppresses the expression of dickkopf-1 and -2 and stimulates Wnt signaling, IL-11 appears to mediate at least a part of the effect of mechanical strain on osteoblast differentiation and bone formation. The present study was undertaken to examine the effect of PTH(1-34) and GCs on IL-11 expression in murine primary osteoblasts (mPOBs). PTH(1-34) treatment of mPOBs enhanced IL-11 expression in a time- and dose-dependent manner. PTH(1-34) also stimulated FosB expression and Smad1 phosphorylation, which cooperatively stimulated IL-11 gene transcription. PTH(1-34)-induced Smad1 phosphorylation was mediated via PKC and was abrogated in mPOBs from PKC knockout mice. Dexamethasone suppressed IL-11 gene transcription enhanced by PTH(1-34) without affecting FosB expression or Smad1 phosphorylation, and dexamethasone-GC receptor complex was bound to JunD, which forms heterodimers with FosB. High doses of PTH(1-34) counteracted the effect of dexamethasone on apoptosis of mPOBs, which was blunted by neutralizing anti-IL-11 antibody or IL-11 small interfering RNA. These results demonstrate that PTH(1-34) and GCs interact to regulate IL-11 expression in parallel with osteoblast differentiation and apoptosis and suggest that PTH(1-34) and dexamethasone may regulate osteoblast differentiation and apoptosis via their effect on IL-11 expression.  (日)    [継承]
キーワード (推奨): 1. (英) Alkaline Phosphatase (日) (読) [継承]
2. (英) Animals (日) (読) [継承]
3. (英) Apoptosis (日) (読) [継承]
4. (英) Cell Differentiation (日) (読) [継承]
5. (英) Cells, Cultured (日) (読) [継承]
6. (英) Dexamethasone (日) (読) [継承]
7. (英) Gene Expression Regulation (日) (読) [継承]
8. (英) Interleukin-11 (日) (読) [継承]
9. (英) Mice (日) (読) [継承]
10. (英) Osteoblasts (日) (読) [継承]
11. (英) Osteocalcin (日) (読) [継承]
12. (英) Osteoprotegerin (日) (読) [継承]
13. (英) Parathyroid Hormone (日) (読) [継承]
14. (英) Phosphorylation (日) (読) [継承]
15. (英) Promoter Regions, Genetic (日) (読) [継承]
16. (英) Protein Kinase C-delta (日) (読) [継承]
17. (英) Proto-Oncogene Proteins c-fos (日) (読) [継承]
18. (英) Proto-Oncogene Proteins c-jun (日) (読) [継承]
19. (英) RANK Ligand (日) (読) [継承]
20. (英) RNA, Messenger (日) (読) [継承]
21. (英) RNA, Small Interfering (日) (読) [継承]
22. (英) Receptors, Glucocorticoid (日) (読) [継承]
23. (英) Signal Transduction (日) (読) [継承]
24. (英) Smad1 Protein (日) (読) [継承]
発行所 (推奨):
誌名 (必須): Endocrinology ([The Endocrine Society])
(pISSN: 0013-7227, eISSN: 1945-7170)

ISSN (任意): 1945-7170
ISSN: 0013-7227 (pISSN: 0013-7227, eISSN: 1945-7170)
Title: Endocrinology
Title(ISO): Endocrinology
Publisher: Endocrine Society
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
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(必須): 154 [継承]
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年月日 (必須): 西暦 2013年 2月 8日 (平成 25年 2月 8日) [継承]
URL (任意):
DOI (任意): 10.1210/en.2013-1915    (→Scopusで検索) [継承]
PMID (任意): 23397032    (→Scopusで検索) [継承]
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備考 (任意): 1.(英) Affiliation: MD, Department of Medicine and Bioregulatory Sciences, University of Tokushima Graduate School of Medicine, 3-18-15 Kuramoto-cho, Tokushima 770-8503, 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]

標準的な表示

和文冊子 ● Rika Kuriwaka-Kido, Shinsuke Kido, Yuka Miyatani, Yuji Ito, Takeshi Kondo, Takashi Omatsu, Bingzi Dong, Itsuro Endo, Ken-ichi Miyamoto and Toshio Matsumoto : Parathyroid hormone (1-34) counteracts the suppression of interleukin-11 expression by glucocorticoid in murine osteoblasts: a possible mechanism for stimulating osteoblast differentiation against glucocorticoid excess., Endocrinology, Vol.154, No.3, 1156-1167, 2013.
欧文冊子 ● Rika Kuriwaka-Kido, Shinsuke Kido, Yuka Miyatani, Yuji Ito, Takeshi Kondo, Takashi Omatsu, Bingzi Dong, Itsuro Endo, Ken-ichi Miyamoto and Toshio Matsumoto : Parathyroid hormone (1-34) counteracts the suppression of interleukin-11 expression by glucocorticoid in murine osteoblasts: a possible mechanism for stimulating osteoblast differentiation against glucocorticoid excess., Endocrinology, Vol.154, No.3, 1156-1167, 2013.

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