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Title: Nardilysin regulates inflammation, metaplasia, and tumors in murine stomach
Authors: Kimura, Yuto
Ikuta, Kozo
Kimura, Takeshi  kyouindb  KAKEN_id
Chiba, Tsutomu
Oshima, Hiroko
Oshima, Masanobu
Nishi, Eiichiro
Seno, Hiroshi  kyouindb  KAKEN_id
Author's alias: 木村, 勇斗
生田, 耕三
木村, 剛
千葉, 勉
西, 英一郎
妹尾, 浩
Keywords: Chronic inflammation
Gastritis
Issue Date: 23-Feb-2017
Publisher: Springer Nature
Journal title: Scientific Reports
Volume: 7
Thesis number: 43052
Abstract: Chronic inflammation contributes to a wide variety of human disorders. In the stomach, longstanding gastritis often results in structural alterations in the gastric mucosa, including metaplastic changes and gastric cancers. Therefore, it is important to elucidate factors that are involved in gastric inflammation. Nardilysin (N-arginine dibasic convertase; Nrdc) is a metalloendopeptidase of the M16 family that promotes ectodomain shedding of the precursor forms of various growth factors and cytokines by enhancing the protease activities of a disintegrin and metalloproteinase (ADAM) proteins. Here, we have demonstrated that Nrdc crucially regulates gastric inflammation caused by Helicobacter felis infection or forced expression of prostaglandin E2 in K19-C2mE mice. Metaplastic changes following gastric inflammation were suppressed by the deletion of Nrdc. Furthremore, the deletion of Nrdc significantly suppressed N-methyl-N-nitrosourea (MNU)-induced gastric tumorigenesis in the murine stomach. These data may lead to a global therapeutic approach against various gastric disorders by targeting Nrdc.
Rights: © The Author(s) 2017
This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material.
URI: http://hdl.handle.net/2433/227670
DOI(Published Version): 10.1038/srep43052
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