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  1. 学位論文
  2. 歯学研究科
  3. 平成29年度
  4. 課程博士

Effects of NOD1 in Human Dental Pulp Fibroblast Like cells

https://osaka-dent.repo.nii.ac.jp/records/191
https://osaka-dent.repo.nii.ac.jp/records/191
e6e88365-5ad4-4bb2-8ffd-f0944590d36b
名前 / ファイル ライセンス アクション
kou_829_txt.pdf 学位論文 (435.2 kB)
kou_829.pdf 論文内容要旨・審査結果要旨 (210.0 kB)
Item type 学位論文 / Thesis or Dissertation(1)
公開日 2018-05-17
本文言語
言語 eng
タイトル
タイトル Effects of NOD1 in Human Dental Pulp Fibroblast Like cells
著者 岩佐, 一弘

× 岩佐, 一弘

岩佐, 一弘

ja-Kana イワサ, カズヒロ

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キーワード
主題Scheme Other
主題 Matrix metalloproteinase-3
キーワード
主題Scheme Other
主題 NOD1
キーワード
主題Scheme Other
主題 iE-DAP
キーワード
主題Scheme Other
主題 JNK
キーワード
主題Scheme Other
主題 RIP2
キーワード
主題Scheme Other
主題 Human pulp fibroblasts
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_db06
資源タイプ doctoral thesis
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
抄録
内容記述タイプ Abstract
内容記述 Purpose: Caries-related immune response is first recognized by dental pulp fibroblast cells and is tightly regulated to avert pulpitis. Nucleotide-binding oligomerization domain (NOD) 1 signaling, which is essential for initiating the innate immune response to bacterial infection, is subject to many regulatory mechanisms. However, little is known about post transcriptional regulation of NOD1 dependent responses in dental pulp fibroblast cells. NOD1 recognizes D-glutamyl-meso-diaminopimelic acid (iE-DAP). RIP2 is associated with NOD1 and play critical roles in the immune system. Matrix metalloproteinases (MMPs) such as MMP-1, 2, 3, and 14 were also shown to be expressed in inflamed dental pulp tissue. MMP-3 can degrade the extracellular matrix (ECM) and activate other MMPs. MMP-3 is considered to be involved in wound healing, inflammation, and tumor initiation. Dental pulp destruction may be regulated, in part, by matrix metalloproteinase-3 (MMP-3), and other MMPs activated by MMP-3 have been shown to regulate the degradation and regeneration of dental pulp tissue. In the present study, we investigated that MMP-3 was produced in response to iE-DAP and cell signaling in human pulp fibroblasts (HPFs).
Methods: HPFs were incubated in serum-free α-MEM containing iE-DAP (10 g/mL) for 24 h with or without the RIP inhibitor, 0.5, 1, 5, 10, 15, 20 nM Gefitinib. The production of MMP-3 and expression of RIP2 were evaluated by RIP2 and MMP-3 antibodies using western blot analysis. HPFs were incubated in serum-free α-MEM containing iE-DAP (10 g/mL) for 24 h with or without the JNK inhibitor, AS601245 or SP600125. The production of MMP-3 and activation of JNK by iE-DAP were evaluated by the phosphorylation of JNK and MMP-3 antibodies using western blot analysis.
Results: iE-DAP enhanced the production of MMP-3 in a dose dependent manner in HPFs. RIP2 inhibitor suppressed the production of MMP-3 on iE-DAP stimulated HPFs. We demonstrated that MMP-3 was produced from HPFs in response to iE-DAP in a JNK-dependent manner.
Conclusion: These results suggest that iE-DAP/NOD1 induced the production of MMP-3 in HPFs through a signaling cascade involving RIP2-mediated phosphorylation of JNK.
学位名
学位名 博士(歯学)
学位授与機関
学位授与機関識別子Scheme kakenhi
学位授与機関識別子 34408
学位授与機関名 大阪歯科大学
学位授与年月日
学位授与年月日 2018-03-09
学位授与番号
学位授与番号 甲第829号
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