Indirect regulation of PCSK9 gene in inflammatory response by Porphyromonas gingivalis infection

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Indirect regulation of PCSK9 gene in inflammatory response by Porphyromonas gingivalis infection

Persistent ID (NDL): info:ndljp/pid/11337465

Material type: 博士論文

Author: Takeuchi, Mai

Publisher: 新潟大学

Date granted: 2019-03-25

Material Format: Digital

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Degree grantor and degree: 新潟大学,博士（歯学）

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Note (General)：: Pro-protein convertase subtilisin/kexin type 9 (PCSK9), a secreted serine protease, regulates serum low-density lipoprotein (LDL) cholesterol levels b...

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Material Type: 博士論文
Title: Indirect regulation of PCSK9 gene in inflammatory response by Porphyromonas gingivalis infection
Author/Editor: Takeuchi, Mai
Publication, Distribution, etc.: 新潟大学
Publication Date: 2019-03-25
Publication Date (W3CDTF): 2019-03-25
Alternative Title: Indirect regulation of PCSK9 gene in inflammatory response by Porphyromonas gingivalis infection
Porphyromonas gingivalis感染時炎症応答におけるPCSK9遺伝子発現の制御機構
Degree Grantor: 新潟大学
Date Granted: 2019-03-25
Date Granted (W3CDTF): 2019-03-25
Dissertation Number: 甲第4575号
Degree Type: 博士（歯学）
Conferring No. (Dissertation): 甲第4575号
Text Language Code: eng
Subject Heading: Immunology
Note (General): Pro-protein convertase subtilisin/kexin type 9 (PCSK9), a secreted serine protease, regulates serum low-density lipoprotein (LDL) cholesterol levels by targeting the degradation of LDL receptor (LDLR) in the liver. Although previous reports describe elevated levels of PCSK9 in patients with periodontitis, the mechanisms that trigger this increase in serum PCSK9 levels and induce the related inflammatory response remain unclear. In an unc93b1-deficient mouse of Porphyromonas gingivalis infection, nucleic acid antigen recognition via Tolllike receptors was found to promote PCSK9 production, suggesting an indirect role for tumor necrosis factor-α as an inducer of PCSK9 in contrast to that reported in previous studies. Furthermore, PCSK9 production was independent of the TIR domain-containing adapter-inducing interferon-β-dependent signaling pathway. These results indicate that changes in LDLR expression precede an increase in the serum PCSK9 level in the context of an infectious disease such as periodontitis.
学位の種類: 博士（歯学）. 報告番号: 甲第4575号. 学位記番号: 新大院博（歯）甲第424号. 学位授与年月日: 平成31年3月25日
Heliyon. 2019, 5(2), e01210
新大院博（歯）甲第424号
元資料の権利情報 : 【○!C】 2018 The Authors. Published by Elsevier Ltd.
開始ページ : 1
終了ページ : 14
DOI: info:doi/10.1016/j.heliyon.2018.e01111
https://doi.org/info:doi/10.1016/j.heliyon.2018.e01111
Persistent ID (NDL): info:ndljp/pid/11337465
https://dl.ndl.go.jp/pid/11337465
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): 2019-08-03T12:23:27+09:00
Date Created (W3CDTF): 2019-09-10
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://hdl.handle.net/10191/51341
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