Effects of Intermittent or Continuous Gravitational Stresses on Cell–Matrix Adhesion: Quantitative Analysis of Focal Contacts in Osteoblastic ROS 17/2.8 Cells

1997 ◽  
Vol 236 (1) ◽  
pp. 66-75 ◽  
Author(s):  
Alain Guignandon ◽  
Yves Usson ◽  
Norbert Laroche ◽  
Marie-Hélène Lafage-Proust ◽  
Odile Sabido ◽  
...  
Keyword(s):  
Quantitative Analysis ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Focal Contacts ◽  
Cell Matrix Adhesion

scholarly journals Probing mechanical principles of focal contacts in cell–matrix adhesion with a coupled stochastic–elastic modelling framework

2011 ◽  
Vol 8 (62) ◽  
pp. 1217-1232 ◽  
Author(s):  
Huajian Gao ◽  
Jin Qian ◽  
Bin Chen
Keyword(s):  
Numerical Models ◽  
Focal Adhesions ◽  
Point Of View ◽  
Matrix Adhesion ◽  
Modelling Framework ◽  
Cell Matrix ◽  
Focal Contacts ◽  
Wide Range ◽  
Sense And Respond ◽  
Cell Matrix Adhesion

Cell–matrix adhesion depends on the collective behaviours of clusters of receptor–ligand bonds called focal contacts between cell and extracellular matrix. While the behaviour of a single molecular bond is governed by statistical mechanics at the molecular scale, continuum mechanics should be valid at a larger scale. This paper presents an overview of a series of recent theoretical studies aimed at probing the basic mechanical principles of focal contacts in cell–matrix adhesion via stochastic–elastic models in which stochastic descriptions of molecular bonds and elastic descriptions of interfacial traction–separation are unified in a single modelling framework. The intention here is to illustrate these principles using simple analytical and numerical models. The aim of the discussions is to provide possible clues to the following questions: why does the size of focal adhesions (FAs) fall into a narrow range around the micrometre scale? How can cells sense and respond to substrates of varied stiffness via FAs? How do the magnitude and orientation of mechanical forces affect the binding dynamics of FAs? The effects of cluster size, cell–matrix elastic modulus, loading direction and cytoskeletal pretension on the lifetime of FA clusters have been investigated by theoretical arguments as well as Monte Carlo numerical simulations, with results showing that intermediate adhesion size, stiff substrate, cytoskeleton stiffening, low-angle pulling and moderate cytoskeletal pretension are factors that contribute to stable FAs. From a mechanistic point of view, these results provide possible explanations for a wide range of experimental observations and suggest multiple mechanisms by which cells can actively control adhesion and de-adhesion via cytoskeletal contractile machinery in response to mechanical properties of their surroundings.

scholarly journals Interaction between Galectin-3 and Integrins Mediates Cell-Matrix Adhesion in Endothelial Cells and Mesenchymal Stem Cells

2021 ◽  
Vol 22 (10) ◽  
pp. 5144
Author(s):  
Antonín Sedlář ◽  
Martina Trávníčková ◽  
Pavla Bojarová ◽  
Miluše Vlachová ◽  
Kristýna Slámová ◽  
...  
Keyword(s):  
Stem Cells ◽  
Endothelial Cells ◽  
Cell Adhesion ◽  
Vascular Tissue ◽  
Cell Functions ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Selective Ligand ◽  
Galectin 3 ◽  
Cell Matrix Adhesion

Galectin-3 (Gal-3) is a β-galactoside-binding protein that influences various cell functions, including cell adhesion. We focused on the role of Gal-3 as an extracellular ligand mediating cell-matrix adhesion. We used human adipose tissue-derived stem cells and human umbilical vein endothelial cells that are promising for vascular tissue engineering. We found that these cells naturally contained Gal-3 on their surface and inside the cells. Moreover, they were able to associate with exogenous Gal-3 added to the culture medium. This association was reduced with a β-galactoside LacdiNAc (GalNAcβ1,4GlcNAc), a selective ligand of Gal-3, which binds to the carbohydrate recognition domain (CRD) in the Gal-3 molecule. This ligand was also able to detach Gal-3 newly associated with cells but not Gal-3 naturally present on cells. In addition, Gal-3 preadsorbed on plastic surfaces acted as an adhesion ligand for both cell types, and the cell adhesion was resistant to blocking with LacdiNAc. This result suggests that the adhesion was mediated by a binding site different from the CRD. The blocking of integrin adhesion receptors on cells with specific antibodies revealed that the cell adhesion to the preadsorbed Gal-3 was mediated, at least partially, by β1 and αV integrins—namely α5β1, αVβ3, and αVβ1 integrins.

scholarly journals Cell–matrix adhesion

2007 ◽  
Vol 213 (3) ◽  
pp. 565-573 ◽  
Author(s):  
Allison L. Berrier ◽  
Kenneth M. Yamada
Keyword(s):  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion

scholarly journals Cell-matrix adhesion controls Golgi organization and function by regulating Arf1 activation in anchorage dependent cells

2018 ◽  
Author(s):  
Vibha Singh ◽  
Chaitanya Erady ◽  
Nagaraj Balasubramanian
Keyword(s):  
Membrane Trafficking ◽  
Microtubule Network ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Summary Statement ◽  
Golgi Fragmentation ◽  
And Function ◽  
Golgi Organization ◽  
Cell Matrix Adhesion ◽  
Constitutively Active

AbstractCell-matrix adhesion regulates membrane trafficking to control anchorage-dependent signaling. While a dynamic Golgi complex can contribute to this pathway, its control by adhesion remains untested. We find the loss of adhesion rapidly disorganizes the Golgi in mouse and human fibroblast cells, its integrity restored rapidly on re-adhesion to fibronectin (but not poly-l-lysine coated beads) along the microtubule network. Adhesion regulates the trans-Golgi more prominently than the cis /cis-medial Golgi, though they show no fallback into the ER making this reorganization distinct from known Golgi fragmentation. This is controlled by an adhesion-dependent drop and recovery of Arf1 activation, mediated through the Arf1 GEF BIG1/2 over GBF1. Constitutively active Arf1 disrupts this regulation and prevents Golgi disorganization in non-adherent cells. Adhesion regulates active Arf1 binding to the microtubule minus-end motor protein dynein to control Golgi reorganization, which ciliobrevin blocks. This regulation by adhesion controls Golgi function, promoting cell surface glycosylation on the loss of adhesion that constitutively active Arf1 blocks. This study hence identifies cell-matrix adhesion to be a novel regulator of Arf1 activation, controlling Golgi organization and function in anchorage-dependent cells.Summary StatementThis study identifies a role for cell-matrix adhesion in regulating organelle (Golgi) architecture and function which could have implications for multiple cellular pathways and function.

scholarly journals Switching between individual and collective motility in B lymphocytes is controlled by cell-matrix adhesion and inter-cellular interactions

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Javier Rey-Barroso ◽  
Daniel S. Calovi ◽  
Maud Combe ◽  
Yolla German ◽  
Mathieu Moreau ◽  
...  
Keyword(s):  
B Lymphocytes ◽  
Cellular Interactions ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion
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