Elucidating the molecular bases and pathophysiological significances of the extracellular inflammasome which drives chronic inflammation

2016 Fiscal Year Final Research Report

• Project/Area Number: 15H06785
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Applied pharmacology
• Research Institution: Shujitsu University
• Principal Investigator: Watanabe Masahiro 就実大学, 薬学部, 助教 (10758246)
• Research Collaborator: MORI Shuji 就実大学, 薬学部, 教授 (50220009) ; TOYOMURA Takao 就実大学, 薬学部, 講師 (40425137)
• Project Period (FY): 2015-08-28 – 2017-03-31
• Keywords: 慢性炎症 / HMGB1 / 終末糖化産物 / AGEs

Outline of Final Research Achievements

To elucidate the mechanisms that HMGB1 or advanced glycation endproducts (AGEs) induce chronic inflammation, we searched for interaction partners of these molecules and investigated the effects induced by the interaction of the molecules. We found that AGEs directly interact with a cytokine, TWEAK. Furthermore, using cellular model, it was shown that AGEs inhibited function of TWEAK which regulate TNFα-stimulated inflammatory reactions. These results suggested that AGEs induce chronic inflammation through inhibiting function of the cytokines which regulate inflammatory reactions.

Free Research Field

薬理学，分子生物学