Flow induced adherens junction remodeling driven by cytoskeletal forces
Autor: | Vivek K. Bajpai, Susan Z. Hua, Deepika Verma, Stelios T. Andreadis, Mohammad Mehdi Maneshi, Deekshitha Jetta, Frederick Sachs, Nannan Ye |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Pyridines Biosensing Techniques Biology Mechanotransduction Cellular Madin Darby Canine Kidney Cells Adherens junction 03 medical and health sciences Dogs Live cell imaging Fluorescence Resonance Energy Transfer Shear stress Animals Actinin Mechanotransduction Cytoskeleton Protein Kinase Inhibitors rho-Associated Kinases Cadherin Wild type Adherens Junctions Cell Biology Cadherins Amides Actins Biomechanical Phenomena Cell biology Actin Cytoskeleton 030104 developmental biology Gene Expression Regulation Stress Mechanical Rheology Transduction (physiology) |
Zdroj: | Experimental Cell Research. 359:327-336 |
ISSN: | 0014-4827 |
Popis: | Adherens junctions (AJs) are a key structural component for tissue organization and function. Under fluid shear stress, AJs exhibit dynamic assembly/disassembly, but how shear stress couples to AJs is unclear. In MDCK cells we measured simultaneously the forces in cytoskeletal α-actinin and the density and length of AJs using a genetically coded optical force sensor, actinin-sstFRET, and fluorescently labeled E-cadherin (E-cad). We found that shear stress of 0.74 dyn/cm2 for 3 h significantly enhanced E-cad expression at cell-cell contacts and this phenomenon has two phases. The initial formation of segregated AJ plaques coincided with a decrease in cytoskeletal tension, but an increase in tension was necessary for expansion of the plaques and the formation of continuous AJs in the later phase. The changes in cytoskeletal tension and reorganization appear to be an upstream process in response to flow since it occurred in both wild type and dominant negative E-cad cells. Disruption of F-actin with a Rho-ROCK inhibitor eliminated AJ growth under flow. These results delineate the shear stress transduction paths in cultured cells, which helps to understand pathology of a range of diseases that involve dysfunction of E-cadherin. |
Databáze: | OpenAIRE |
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