Transient/sustained activation of pro-inflammatory signaling that depends on cellular mechanical forces

2014 Fiscal Year Final Research Report

• Project/Area Number: 24680049
• Research Category: Grant-in-Aid for Young Scientists (A)
• Allocation Type: Partial Multi-year Fund
• Research Field: Biomedical engineering/Biological material science
• Research Institution: Nagoya Institute of Technology (2013-2014); Tohoku University (2012)
• Principal Investigator: DEGUCHI Shinji 名古屋工業大学, 工学(系)研究科(研究院), 准教授 (30379713)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 張力ホメオスタシス / 適応 / メカノコントローラー / メカノバイオロジー / 非筋II型ミオシン / 焦点接着斑

Outline of Final Research Achievements

Inflammation is associated with the immune response in the body, but here we hypothesize that pro-inflammatory signaling within tissue cells is regulated by mechanical forces in a manner independent of the immune response. We particularly focus on a particular protein, paxillin, which constitutes cell–substrate adhesions or focal adhesions where cellular contractile forces are constantly exerted. Tyrosine phosphorylation of paxillin is significantly increased upon reduction in cellular contractile forces, which then activates rac1 and induces pro-inflammatory response. These results show that cells exhibit chronic and transient activation of pro-inflammatory response in the absence and presence of contractile forces, respectively.

Free Research Field

生体医工学