scholarly journals Mechanical Stress Modulation: Modulation of Mechanical Stress Mitigates Anti‐Dsg3 Antibody‐Induced Dissociation of Cell–Cell Adhesion (Adv. Biology 1/2021)

2021 ◽  
Vol 5 (1) ◽  
pp. 2170014
Author(s):  
Xiaowei Jin ◽  
Jordan Rosenbohm ◽  
Eunju Kim ◽  
Amir Monemian Esfahani ◽  
Kristina Seiffert‐Sinha ◽  
...  
2021 ◽  
pp. 2000159
Author(s):  
Xiaowei Jin ◽  
Jordan Rosenbohm ◽  
Eunju Kim ◽  
Amir Monemian Esfahani ◽  
Kristina Seiffert‐Sinha ◽  
...  

2021 ◽  
Author(s):  
Shafali Gupta ◽  
Kinga Duszyc ◽  
Suzie Verma ◽  
Srikanth Budnar ◽  
Xuan Liang ◽  
...  

Epithelia migrate as physically coherent populations of cells. Earlier studies revealed that mechanical stress accumulates in these cellular layers as they move. These stresses are characteristically tensile in nature and have often been inferred to arise when moving cells pull upon the cell-cell adhesions that hold them together. We now report that epithelial tension at adherens junctions between migrating cells also reflects an increase in RhoAmediated junctional contractility. We find that active RhoA levels were stimulated by p114 RhoGEF at the junctions between migrating MCF-7 monolayers, and this is accompanied by increased levels of actomyosin and mechanical tension. By applying a strategy to restore active RhoA specifically at adherens junctions by manipulating its scaffold, anillin, we found that this junctional RhoA signal was necessary to stabilize junctional E-cadherin during epithelial migration. We suggest that stabilization of E-cadherin by RhoA serves to increase cell-cell adhesion against the mechanical stresses of migration.


2021 ◽  
Author(s):  
Shafali Gupta ◽  
Kinga Duszyc ◽  
Suzie Verma ◽  
Srikanth Budnar ◽  
Xuan Liang ◽  
...  

Epithelia migrate as physically coherent populations of cells. Earlier studies revealed that mechanical stress accumulates in these cellular layers as they move. These stresses are characteristically tensile in nature and have often been inferred to arise when moving cells pull upon the cell-cell adhesions that hold them together. We now report that epithelial tension at adherens junctions between migrating cells also increases due to an increase in RhoA-mediated junctional contractility. We find that active RhoA levels were stimulated by p114 RhoGEF at the junctions between migrating MCF-7 monolayers, and this was accompanied by increased levels of actomyosin and mechanical tension. Applying a strategy to restore active RhoA specifically at adherens junctions by manipulating its scaffold, anillin, we found that this junctional RhoA signal was necessary to stabilize junctional E-cadherin during epithelial migration and promoted orderly collective movement. We suggest that stabilization of E-cadherin by RhoA serves to increase cell-cell adhesion against the mechanical stresses of migration.


2005 ◽  
Vol 173 (4S) ◽  
pp. 170-170
Author(s):  
Maxine G. Tran ◽  
Miguel A. Esteban ◽  
Peter D. Hill ◽  
Ashish Chandra ◽  
Tim S. O'Brien ◽  
...  

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