The distinct roles of myosin IIA and IIB under compression stress in nucleus pulposus cells. (7th January 2021)

• Record Type: Journal Article
• Authors: Ke, Wencan; Wang, Bingjin; Hua, Wenbin; Song, Yu; Lu, Saideng; Luo, Rongjin; Li, Gaocai; Wang, Kun; Liao, Zhiwei; Xiang, Qian; Li, Shuai; Wu, Xinghuo; Zhang, Yukun; Yang, Cao
• Is Part Of: Cell proliferation. Volume 54:Number 2(2021)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2021-01-07
• Subjects: actomyosin cytoskeleton -- compression stress -- intervertebral disc degeneration -- myosin II -- RhoA/ROCK; Cell proliferation -- Periodicals; 571.84
• DOI: 10.1111/cpr.12987
• Languages: English
• ISSNs: 0960-7722

Abstract

Abstract: Objectives: Inappropriate or excessive compression applied to intervertebral disc (IVD) contributes substantially to IVD degeneration. The actomyosin system plays a leading role in responding to mechanical stimuli. In the present study, we investigated the roles of myosin II isoforms in the compression stress‐induced senescence of nucleus pulposus (NP) cells. Material and methods: Nucleus pulposus cells were exposed to 1.0 MPa compression for 0, 12, 24 or 36 hours. Immunofluorescence and co‐immunoprecipitation analysis were used to measure the interaction of myosin IIA and IIB with actin. Western blot analysis and immunofluorescence staining were used to detect nuclear expression and nuclear localization of MRTF‐A. In addition, the expression levels of p‐RhoA/RhoA, ROCK1/2 and p‐MLC/MLC were measured in human NP cells under compression stress and in degenerative IVD tissues. Results: Compression stress increased the interaction of myosin IIA and actin, while the interaction of myosin IIB and actin was reduced. The actomyosin cytoskeleton remodelling was involved in the compression stress‐induced fibrotic phenotype mediated by MRTF‐A nuclear translocation and inhibition of proliferation in NP cells. Furthermore, RhoA/ROCK1 pathway activation mediated compression stress‐induced human NP cells senescence by regulating the interaction of myosin IIA and IIB with actin. Conclusions: We for the first time investigated the regulation of actomyosin cytoskeleton in human NP cells under compression stress. It provided new insights into the development of therapy for effectively inhibiting IVD degeneration. Abstract : Compression stress induced the RhoA/ROCK1 pathway activation, which regulated the interaction of myosin IIA and IIB with actin. The actomyosin cytoskeleton remodelling was involved in the compression stress‐induced fibrotic phenotype mediated by MRTF‐A nuclear translocation and inhibition of proliferation in human NP cells.