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Related Concept Videos

Tension Response at Adherens Junctions01:26

Tension Response at Adherens Junctions

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The adherens junctions that anchor cells together are multi-protein complexes that dynamically adapt to mechanical stimuli such as tensile forces and shear stress. Mechanosensory proteins in these junctions can sense such mechanical stimuli and undergo a shift in their conformation, resulting in an altered function — a process called mechanotransduction.
α-Catenin as a Mechanosensory Protein
The α-catenin of adherens junctions is an allosteric protein with three VH (vinculin...
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In animal cells, the extracellular matrix allows cells within tissues to withstand external stresses and transmits signals from the outside of the cell to the inside. The extracellular matrix is extensive, and its composition varies between different types of tissues. For example, the reticular fibers and ground substance make up the ECM in loose connective tissue, while collagen and bone minerals make up the ECM of bone tissue. 
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Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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Adherens Junctions01:24

Adherens Junctions

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Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
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Blebs are a type of membrane protrusion formed by the internal hydrostatic pressure of the cytoplasm. Blebs are observed in several cell types, including fibroblasts, immune cells, and single-celled organisms like the amoeba. The primary function of blebs is cell locomotion and apoptosis, but they are also found during necrosis and cell division. The life cycle of a bleb comprises an initiation phase followed by the expansion and retraction phases.
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A migrating cell changes its shape during the cyclic events of attachment and detachment from the substratum and repositions the cell organelles correspondingly. These complex events are orchestrated by the dynamic cytoskeletal network comprising actin filaments, intermediate filaments, and microtubules. Cytoskeletal crosstalk — the direct and indirect communication between the different components — is crucial for this coordination. Direct communication involves various linker...
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Analyzing Cell Surface Adhesion Remodeling in Response to Mechanical Tension Using Magnetic Beads
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Flow induced adherens junction remodeling driven by cytoskeletal forces.

Deepika Verma1, Vivek K Bajpai2, Nannan Ye3

  • 1Department of Mechanical and Aerospace Engineering, University at Buffalo, Buffalo, NY 14260, USA; Department of Physiology and Biophysics, University at Buffalo, Buffalo, NY 14260, USA.

Experimental Cell Research
|August 14, 2017
PubMed
Summary

Fluid shear stress dynamically alters adherens junctions (AJs) in two phases, involving cytoskeletal tension changes and F-actin reorganization, crucial for understanding E-cadherin dysfunction in diseases.

Keywords:
Cytoskeletal forceE-cadherinFRETLive cell imagingMDCK cellsMechanotransduction

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Area of Science:

  • Cell biology
  • Biophysics
  • Tissue engineering

Background:

  • Adherens junctions (AJs) are vital for tissue integrity.
  • The mechanism linking fluid shear stress to AJ dynamics remains unclear.

Purpose of the Study:

  • To investigate how fluid shear stress influences adherens junctions.
  • To elucidate the role of cytoskeletal tension in AJ remodeling under flow.

Main Methods:

  • Utilized actinin-sstFRET, a genetically encoded optical force sensor, to measure cytoskeletal forces.
  • Quantified E-cadherin density and length at cell-cell contacts in MDCK cells.
  • Applied fluid shear stress (0.74 dyn/cm² for 3h) and used Rho-ROCK inhibitor.

Main Results:

  • Shear stress induced a biphasic response in E-cadherin expression and AJ formation.
  • Initial AJ plaque formation correlated with decreased cytoskeletal tension; plaque expansion required increased tension.
  • Cytoskeletal tension changes preceded AJ reorganization, independent of E-cadherin levels.
  • Disruption of F-actin abolished AJ growth under shear stress.

Conclusions:

  • Delineated shear stress transduction pathways influencing adherens junctions.
  • Identified cytoskeletal tension and F-actin dynamics as key regulators of AJ remodeling under flow.
  • Provided insights into diseases involving E-cadherin dysfunction.