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2016 Fiscal Year Final Research Report

Analysis of the mechanism responsible for the onset of ulcerative colitis using S100 transgenic rats

Research Project

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Project/Area Number 26460663
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Laboratory medicine
Research InstitutionTenri Health Care University

Principal Investigator

Ikemoto Masaki  天理医療大学, 医療学部, 教授 (80144385)

Project Period (FY) 2014-04-01 – 2017-03-31
Keywordsマクロファージ / トランスジェニックラット / 急性炎症 / LPS / S100タンパク質
Outline of Final Research Achievements

We artificially inserted S100A8 cDNA to the pCXGFP vector and then injected the resultant plasmid to embryonic stem (ES) cells of rats, and conclusively succeeded in having a S100A8 transgenic rat (Tg-S100A8). Lipopolysaccharide (LPS) was intraperitoneally administrated in wild-type rats and Tg-S100A8, so that acute liver damage has been induced in the liver tissue of WT-rats, where many macrophages have been also accumulated. While, acute liver damage in Tg-S100A8 was not almost observed, and immune cells were scattered in the liver tissue. These facts suggest that S100A8 could serve as an anti-inflammatory protein in Tg-S100A8. We are attempting to elucidate the mechanisms responsible for negatively regulating acute liver damage by LPS in Tg-S100A8.

Free Research Field

臨床病態学

URL: 

Published: 2018-03-22  

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