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Elucidation of fibrosis mechanism in inflammatory bowel disease and its application to molecular targeting therapy

Research Project

Project/Area Number 26460976
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Gastroenterology
Research InstitutionYokohama City University

Principal Investigator

SHIBATA Wataru  横浜市立大学, 先端医科学研究センター, 准教授 (00435819)

Project Period (FY) 2014-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywords線維化 / NF-kB / 炎症性腸疾患 / NFkB / NF-kB / 線維芽細胞
Outline of Final Research Achievements

Here we investigated the role of numerous fibroblasts in the inflamed region on fibrosis, focusing on the activation of the expected NF-κB pathway, which is particularly relevant. NF-κB deficient mice specific for myofibroblasts considered to be involved in fibrosis were prepared, and dextran sodium sulfate (DSS) intestinal inflammation model and intestinal allograft model were examined. In vitro studies, we used fetal embryonic fibroblast cells. As a result, the number of myofibroblast cells induced by inflammation was less in knockout mice in intestinal inflammation model. αSMA and TGFβ were attenuated in knockout mice in transplanted intestinal tract. In the examination with MEF, expression of TGFβ and inflammatory cytokine by inflammatory stimulation was decreased in knockout MEF, suggesting that the NF-kB pathway was involved in fibrosis formation.

Report

(4 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report
  • 2014 Research-status Report

URL: 

Published: 2014-04-04   Modified: 2018-03-22  

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