Recruitment of β-Catenin to N-Cadherin Is Necessary for Smooth Muscle Contraction

Wang, Tao; Wang, Ruping; Cleary, Rachel A.; Gannon, Olivia J.; Tang, Dale D.

doi:10.1074/jbc.m114.621003

Cited by 43 publications

(55 citation statements)

References 51 publications

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“…2D & 3A). These findings are inline with independent reports that the recruitment of β-catenin to N-cadherin is an integral part of the force transmission machinery in healthy airways 29 . As ECM stiffness was increased (E=13kPa), we found that there was a significant decrease in cell-cell coupling strength.…”

Section: Discussionsupporting

confidence: 91%

Extracellular matrix stiffness regulates force transmission pathways in multicellular ensembles of human airway smooth muscle cells

Polio

Stasiak

Krishnan

et al. 2018

Preprint

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For an airway or a blood vessel to narrow, there must be a connected path that links the smooth muscle (SM) cells with each other, and transmits forces around the organ, causing it to constrict. Currently, we know very little about the mechanisms that regulate force transmission pathways in a multicellular SM ensemble. Here, we used extracellular matrix (ECM) micropatterning to study force transmission in a two-cell ensemble of SM cells. Using the two-SM cell ensemble, we demonstrate (a) that ECM stiffness acts as a switch that regulates whether SM force is transmitted through the ECM or through cell-cell connections. (b) Fluorescent imaging for adherens junctions and focal adhesions show the progressive loss of cell-cell borders and the appearance of focal adhesions with the increase in ECM stiffness (confirming our mechanical measurements). (c) At the same ECM stiffness, we show that the presence of a cell-cell border substantially decreases the overall contractility of the SM cell ensemble. Our results demonstrate that connectivity among SM cells is a critical factor to consider in the development of diseases such as asthma and hypertension.

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Section: Discussionsupporting

confidence: 91%

Extracellular matrix stiffness regulates force transmission pathways in multicellular ensembles of human airway smooth muscle cells

Polio

Stasiak

Krishnan

et al. 2018

Preprint

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“…In addition, actin dynamics is able to promote the recruitment of β-catenin to N-cadherin in smooth muscle, which strengthens the cadherin-mediated intercellular linkage [2, 26]. Cadherin-mediated cell-cell adhesion facilitates collective cell migration and development [27].…”

Section: Roles Of Dynamic Actin Cytoskeleton and Actin-associated Promentioning

confidence: 99%

The roles and regulation of the actin cytoskeleton, intermediate filaments and microtubules in smooth muscle cell migration

2017

Self Cite

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Smooth muscle cell migration has been implicated in the development of respiratory and cardiovascular systems; and airway/vascular remodeling. Cell migration is a polarized cellular process involving a protrusive cell front and a retracting trailing rear. There are three cytoskeletal systems in mammalian cells: the actin cytoskeleton, the intermediate filament network, and microtubules; all of which regulate all or part of the migrated process. The dynamic actin cytoskeleton spatially and temporally regulates protrusion, adhesions, contraction, and retraction from the cell front to the rear. c-Abl tyrosine kinase plays a critical role in regulating actin dynamics and migration of airway smooth muscle cells and nonmuscle cells. Recent studies suggest that intermediate filaments undergo reorganization during migration, which coordinates focal adhesion dynamics, cell contraction, and nucleus rigidity. In particular, vimentin intermediate filaments undergo phosphorylation and reorientation in smooth muscle cells, which may regulate cell contraction and focal adhesion assembly/disassembly. Motile cells are characterized by a front-rear polarization of the microtubule framework, which regulates all essential processes leading to cell migration through its role in cell mechanics, intracellular trafficking, and signaling. This review recapitulates our current knowledge how the three cytoskeletal systems spatially and temporally modulate the migratory properties of cells. We also summarize the potential role of migration-associated biomolecules in lung and vascular diseases.

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“…In this respect, Wang et al . () showed that the recruitment of β‐catenin to N‐cadherin AJs is enhanced by ACh stimulation of human airway smooth muscle cells, providing additional evidence of inside‐out signalling modulating the function of N‐cadherin AJs in airway smooth muscle. Interestingly, in their study, the recruitment of β‐catenin was dependent on actin polymerization but not on myosin II activity or microtubule polymerization.…”

Section: Discussionmentioning

confidence: 86%

N‐Cadherin, a novel and rapidly remodelling site involved in vasoregulation of small cerebral arteries

Sun

Li²,

Li³

et al. 2017

The Journal of Physiology

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N-cadherin is the major cell-cell adhesion molecule in vascular smooth muscle cells (VSMCs). We tested the hypothesis that N-cadherin is part of a novel mechanosensory mechanism in VSMCs and plays an active role in both the arteriolar myogenic response and during changes in vascular tone induced by vasomotor agonists. Intact and pressurized rat superior cerebellar arteries were labelled for confocal immunofluorescence imaging. N-cadherin formed punctate adherens junctions (AJ) along the borders between VSMCs. When the lumen pressure was raised from 50 to 90 mmHg, both the density and the average size of N-cadherin AJs increased significantly. Similarly, arteriolar constriction with phenylephrine (PE) (10 m) induced a significant increase of N-cadherin AJ density at 50 mmHg, whereas vasodilatation induced by ACh (10 m) was accompanied by a significant decrease in density and size of N-cadherin AJs. An atomic force microscope (AFM) was employed to further examine the mechano-responsive properties of N-cadherin adhesion sites in isolated VSMCs. AFM probes with an attached N-cadherin-coated microbead (5 μm) induced a progressive clustering of N-cadherin-enhanced green fluorescent protein (EGFP) on the VSMC surface. Application of pulling force (∼1 nN) to the N-cadherin-coated-beads with the AFM induced a localized mechanical response from the VSMCs that opposed the pulling. Treatment with PE (10 m) or sodium nitroprusside (10 m) induced a significant increase or decrease of the N-cadherin-EGFP clustering, respectively. These observations provide compelling evidence that N-cadherin AJs are sensitive to pressure and vasomotor agonists in VSMCs and support a functional role of N-cadherin AJs in vasomotor regulation.

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Recruitment of β-Catenin to N-Cadherin Is Necessary for Smooth Muscle Contraction

Cited by 43 publications

References 51 publications

Extracellular matrix stiffness regulates force transmission pathways in multicellular ensembles of human airway smooth muscle cells

Extracellular matrix stiffness regulates force transmission pathways in multicellular ensembles of human airway smooth muscle cells

The roles and regulation of the actin cytoskeleton, intermediate filaments and microtubules in smooth muscle cell migration

N‐Cadherin, a novel and rapidly remodelling site involved in vasoregulation of small cerebral arteries

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