What is the molecular mechanism of stress fiber disassembly caused by cyclic stretch?

2014 Fiscal Year Final Research Report

• Project/Area Number: 25750154
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Biomedical engineering/Biomaterial science and engineering
• Research Institution: Kyushu Institute of Technology
• Principal Investigator: HUANG Wenjing 九州工業大学, 若手研究者フロンティア研究アカデミー, 研究員 (00633413)
• Research Collaborator: DEGUCHI Shinji 名古屋工業大学, おもひ領域, 准教授 (30379713) ; MATSUI Tsubasa 名古屋工業大学, おもひ領域, 特任助教 (50638707)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: Cyclic stretch / Stress fiber disassembly / Nonmuscle myosin II

Outline of Final Research Achievements

Stress fibers (SFs), which consist of actin filaments and nonmuscle myosin II (NMII), undergo disassembly after cyclic stretch (CS) exposure. CS involves cell lengthening and shortening. I found that fast shorteningof cells that exceeded the intrinsic contraction speed of SFs, but not slow shortening and fast/slow lengthening, caused SF disassembly. Since NMII disassociation from actin occurred in cells exposed to a fast shortening process exceeding the rate of the NMII motion, the results of the study demonstrated that NMII should be involved in the disassembly of SFs in cells, which was further confirmed by basic experiments: SFs whose actin-NMII interactions were restricted were more prone to disassembly upon fast cell shortening. On the other hand, SF disassembly still occurred in cells exposed to CS even in cofilin-inactivated cells. Therefore, the results demonstrate that dissociation of NMII from actin bundles is the primary mechanism for CS-induced SF disassembly.

Free Research Field

医工学