Functional Roles of NOD1 in Odontoblasts on Dental Pulp Innate Immunity

• Material Type: 博士論文
• ISSN: 2314-6133
• Title: Functional Roles of NOD1 in Odontoblasts on Dental Pulp Innate Immunity
• Volume: 2016
• Author/Editor: Hosokawa, Yuki; Hirao, Kouji; Yumoto, Hiromichi; Washio, Ayako; Nakanishi, Tadashi; Takegawa, Daisuke; Kitamura, Chiaki; Matsuo, Takashi
• Author Heading: Hosokawa, Yuki; Hirao, Kouji; Yumoto, Hiromichi; Washio, Ayako; Nakanishi, Tadashi; Takegawa, Daisuke; Kitamura, Chiaki; Matsuo, Takashi
• Publication, Distribution, etc.: Hindawi
• Publication Date: 2016
• Publication Date (W3CDTF): 2016
• Alternative Title: 歯髄象牙芽細胞の自然免疫反応におけるNOD1の役割
• Periodical title: BioMed Research International
• Degree grantor/type: 徳島大学
• Date Granted: 2017-03-23
• Date Granted (W3CDTF): 2017-03-23
• Dissertation Number: 甲第3083号
• Degree Type: 博士（歯学）
• Conferring No. (Dissertation): 甲第3083号
• Text Language Code: eng
• Subject Heading: Odontoblasts; KN-3; NOD1; pulpitis
• Target Audience: 一般
• Note (General): 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.
• DOI: info:doi/10.1155/2016/9325436; https://doi.org/info:doi/10.1155/2016/9325436
• Persistent ID (NDL): info:ndljp/pid/10993565; https://dl.ndl.go.jp/pid/10993565
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2017-12-04T02:02:48+09:00
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Periodical Title (URI): http://repo.lib.tokushima-u.ac.jp/112386
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

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2019-09-09 再収集