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Biophysical journal v.112 no.2, 2017년, pp.388 - 397   SCI SCIE
본 등재정보는 저널의 등재정보를 참고하여 보여주는 베타서비스로 정확한 논문의 등재여부는 등재기관에 확인하시기 바랍니다.

Physical Model for Stabilization and Repair of Trans-endothelial Apertures

Fedorov, Eduard G. (Department of Biology, Israel Institute of Technology, Haifa, Israel ) ; Shemesh, Tom (Department of Biology, Israel Institute of Technology, Haifa, Israel ) ;
  • 초록  

    Abstract Bacterial toxins that disrupt the stability of contractile structures in endothelial cells promote the opening of large-scale apertures, thereby breaching the endothelium barrier. These apertures are formed by fusion of the basal and apical membranes into a tunnel that spans the height of the cell. Subsequent to the aperture formation, an active repair process, driven by a stimulated polymerization of actin, results in asymmetrical membrane protrusions and, ultimately, the closure of the aperture. Here, we propose a physics-based model for the generation, stabilization and repair of trans-endothelial apertures. Our model is based on the mechanical interplay between tension in the plasma membrane and stresses that develop within different actin structures at the aperture’s periphery. We suggest that accumulation of cytoskeletal fragments around the aperture’s rim during the expansion phase results in parallel bundles of actin filaments and myosin motors, generating progressively greater contraction forces that resist further expansion of the aperture. Our results indicate that closure of the tunnel is driven by mechanical stresses that develop within a cross-linked actin gel that forms at localized regions of the aperture periphery. We show that stresses within the gel are due to continuous polymerization of actin filaments against the membrane surfaces of the aperture’s edges. Based on our mechanical model, we construct a dynamic simulation of the aperture repair process. Our model fully accounts for the phenomenology of the trans-endothelial aperture formation and stabilization, and recaptures the experimentally observed asymmetry of the intermediate aperture shapes during closure. We make experimentally testable predictions for localization of myosin motors to the tunnel periphery and of adhesion complexes to the edges of apertures undergoing closure, and we estimate the minimal nucleation size of cross-linked actin gel that can lead to a successful repair of the aperture.


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