Trpm7 Protein Contributes to Intercellular Junction Formation in Mouse Urothelium

Persistent ID (NDL): info:ndljp/pid/10402850

Material type: 博士論文

Author: 渡邊, 成樹

Publisher: -

Publication date: 2015-12

Material Format: Digital

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Name of awarding university/degree: 旭川医科大学,博士（医学）

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Note (General)：: Trpm7 is a divalent cation-permeable channel that has been reported to be involved in magnesium homeostasis as well as cellular adhesion and migration...

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Material Type: 博士論文
Title: Trpm7 Protein Contributes to Intercellular Junction Formation in Mouse Urothelium
Volume: 290 50
Author/Editor: 渡邊, 成樹
Publication Date: 2015-12
Publication Date (W3CDTF): 2015-12
Alternative Title: TRPM7蛋白のマウス尿路上皮細胞間結合の形成への関与
Periodical title: The Journal of biological chemistry.
Degree grantor/type: 旭川医科大学
Date Granted: 2017-06-30
Date Granted (W3CDTF): 2017-06-30
Dissertation Number: 甲第512号
Degree Type: 博士（医学）
Conferring No. (Dissertation): 甲第512号
Text Language Code: eng
Subject Heading: animal model
cell junction
epithelial cell
inflammation
transient receptor potential channels (TRP channels)
Note (General): Trpm7 is a divalent cation-permeable channel that has been reported to be involved in magnesium homeostasis as well as cellular adhesion and migration. We generated urothelium-specific Trpm7 knock-out (KO) mice to reveal the function of Trpm7 in vivo. A Trpm7 KO was induced by tamoxifen and was confirmed by genomic PCR and immunohistochemistry. By using patch clamp recordings in primary urothelial cells, we observed that Mg(2+)-inhibitable cation currents as well as acid-inducible currents were significantly smaller in Trpm7 KO urothelial cells than in cells from control mice. Assessment of voiding behavior indicated a significantly smaller voided volume in Trpm7 KO mice (mean voided volume 0.28 ± 0.08 g in KO mice and 0.36 ± 0.04 g in control mice, p < 0.05, n = 6-8). Histological analysis showed partial but substantial edema in the submucosal layer of Trpm7 KO mice, most likely due to inflammation. The expression of proinflammatory cytokines TNF-α and IL-1β was significantly higher in Trpm7 KO bladders than in controls. In transmission electron microscopic analysis, immature intercellular junctions were observed in Trpm7 KO urothelium but not in control mice. These results suggest that Trpm7 is involved in the formation of intercellular junctions in mouse urothelium. Immature intercellular junctions in Trpm7 knock-out mice might lead to a disruption of barrier function resulting in inflammation and hypersensitive bladder afferent nerves that may affect voiding behavior in vivo.
identifier:PMID：26504086
開始ページ : 29882
終了ページ : 29892
DOI: info:doi/10.1074/jbc.M115.667899
https://doi.org/info:doi/10.1074/jbc.M115.667899
Persistent ID (NDL): info:ndljp/pid/10402850
https://dl.ndl.go.jp/pid/10402850
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): 2017-08-02T04:31:34+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://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20170630_K512
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
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