『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=327689EID:327689, Map:0, LastModified:2018年12月13日(木) 15:27:05, Operator:[三木 ちひろ], Avail:TRUE, Censor:0, Owner:[湯本 浩通], 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): 研究 [継承]
共著種別 (推奨): 国内共著 (徳島大学内研究者と国内(学外)研究者との共同研究 (国外研究者を含まない)) [継承]
学究種別 (推奨): 博士課程学生による研究報告 [継承]
組織 (推奨):
著者 (必須): 1. (英) Hosokawa Yuki (日) (読)
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[継承]
2.平尾 功治
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[継承]
3.湯本 浩通 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.臨床歯学系.歯周歯内治療学])
役割 (任意):
貢献度 (任意):
学籍番号 (推奨):
[継承]
4. (英) Washio Ayako (日) (読)
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[継承]
5.中西 正 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.臨床歯学系.再生歯科治療学]/[徳島大学.病院.診療科.歯科.むし歯科(第一保存科)])
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貢献度 (任意):
学籍番号 (推奨):
[継承]
6.武川 大輔 ([徳島大学.大学院医歯薬学研究部.歯学域.口腔科学部門.臨床歯学系.再生歯科治療学]/[徳島大学.病院.診療科.歯科.むし歯科(第一保存科)])
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貢献度 (任意):
学籍番号 (推奨):
[継承]
7. (英) Kitamura Chiaki (日) (読)
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学籍番号 (推奨):
[継承]
8.松尾 敬志
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学籍番号 (推奨):
[継承]
題名 (必須): (英) Functional roles of NOD1 in odontoblasts on dental pulp innate immunity  (日)    [継承]
副題 (任意):
要約 (任意): (英) Caries-related pathogens are first recognized by odontoblasts and induce inflammatory events that develop to pulpitis. Generally, initial sensing of microbial pathogens is mediated by pattern recognition receptors, such as Toll-like receptor and nucleotide-binding oligomerization domain (NOD); however, little is known about NODs in odontoblasts. In this study, the levels of NODs expressed in rat odontoblastic cell line, KN-3, were assessed by flow cytometry and the levels of chemokines in NOD-specific ligand-stimulated KN-3 cells were analyzed by real-time PCR and ELISA. The signal transduction pathway activated with NOD-specific ligand was assessed by blocking assay with specific inhibitors and reporter assay. In KN-3 cells, the expression level of NOD1 was stronger than that of NOD2 and the production of chemokines, such as CINC-1, CINC-2, CCL20, and MCP-1, was upregulated by stimulation with NOD1-specific ligand, but not with NOD2-specific ligand. CINC-2 and CCL20 production by stimulation with NOD1-specific ligand was reduced by p38 MAPK and AP-1 signaling inhibitors. Furthermore, the reporter assay demonstrated AP-1 activation in NOD1-specific ligand-stimulated KN-3 cells. These findings indicated that NOD1 expressed in odontoblasts functions to upregulate the chemokines expression via p38-AP-1 signaling pathway and suggested that NOD1 may play important roles in the initiation and progression of pulpitis.  (日)    [継承]
キーワード (推奨): 1. (英) Animals (日) (読) [継承]
2. (英) Cell Line (日) (読) [継承]
3.細胞質分裂 (cytokinesis) [継承]
4. (英) Dental Pulp (日) (読) [継承]
5.自然免疫 (innate immunity) [継承]
6. (英) Inflammation Mediators (日) (読) [継承]
7. (英) Nod1 Signaling Adaptor Protein (日) (読) [継承]
8. (英) Odontoblasts (日) (読) [継承]
9. (英) Rats (日) (読) [継承]
発行所 (推奨):
誌名 (必須): BioMed Research International (Hindawi Pub. Co.)
(pISSN: 2314-6133, eISSN: 2314-6141)

ISSN (任意): 2314-6141
ISSN: 2314-6133 (pISSN: 2314-6133, eISSN: 2314-6141)
Title: BioMed research international
Title(ISO): Biomed Res Int
Publisher: Hindawi
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
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(必須): 2016 [継承]
(必須): [継承]
(必須): 9325436 9325436 [継承]
都市 (任意):
年月日 (必須): 西暦 2016年 9月 25日 (平成 28年 9月 25日) [継承]
URL (任意):
DOI (任意): 10.1155/2016/9325436    (→Scopusで検索) [継承]
PMID (任意): 27747243    (→Scopusで検索) [継承]
CRID (任意):
WOS (任意):
Scopus (任意): 2-s2.0-84991669747 [継承]
機関リポジトリ : 112386 [継承]
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備考 (任意): 1.(英) Article.PublicationTypeList.PublicationType: Journal Article  (日)    [継承]
2.(英) CoiStatement: The authors declare that there is no conflict of interest regarding the publication of this paper.  (日)    [継承]

標準的な表示

和文冊子 ● Yuki Hosokawa, Kouji Hirao, Hiromichi Yumoto, Ayako Washio, Tadashi Nakanishi, Daisuke Takegawa, Chiaki Kitamura and Takashi Matsuo : Functional roles of NOD1 in odontoblasts on dental pulp innate immunity, BioMed Research International, Vol.2016, 9325436, 2016.
欧文冊子 ● Yuki Hosokawa, Kouji Hirao, Hiromichi Yumoto, Ayako Washio, Tadashi Nakanishi, Daisuke Takegawa, Chiaki Kitamura and Takashi Matsuo : Functional roles of NOD1 in odontoblasts on dental pulp innate immunity, BioMed Research International, Vol.2016, 9325436, 2016.

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