Cytoskeletal proteins talin and vinculin in integrin-mediated adhesion

The cytoskeletal proteins talin and vinculin form part of a macromolecular complex on the cytoplasmic face of integrin-mediated cellular junctions with the extracellular matrix. Recent genetic, biochemical and structural data show that talin is essential for the assembly of such junctions, whereas vinculin appears to be important in regulating adhesion dynamics and cell migration.

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Neutrophil migration through in vitro interstitial matrix

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100124872 ◽

1992 ◽

Vol 50 (1) ◽

pp. 894-895

Author(s):

J. Roemer ◽

S.R. Simon

Keyword(s):

Extracellular Matrix ◽

Smooth Muscle ◽

Cell Migration ◽

Smooth Muscle Cells ◽

Inflammatory Cell ◽

Neutrophil Migration ◽

Culture Conditions ◽

Aortic Smooth Muscle ◽

Specific Culture

We are developing an in vitro interstitial extracellular matrix (ECM) system for study of inflammatory cell migration. Falcon brand Cyclopore membrane inserts of various pore sizes are used as a support substrate for production of ECM by R22 rat aortic smooth muscle cells. Under specific culture conditions these cells produce a highly insoluble matrix consisting of typical interstitial ECM components, i.e.: types I and III collagen, elastin, proteoglycans and fibronectin.

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Faculty Opinions recommendation of The neural cell adhesion molecule L1 potentiates integrin-dependent cell migration to extracellular matrix proteins.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1009197.119458 ◽

2002 ◽

Author(s):

Genevieve Rougon

Keyword(s):

Extracellular Matrix ◽

Cell Migration ◽

Cell Adhesion ◽

Adhesion Molecule ◽

Cell Adhesion Molecule ◽

Neural Cell Adhesion Molecule ◽

Matrix Proteins ◽

Neural Cell Adhesion ◽

Dependent Cell ◽

Cell Adhesion Molecule L1

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Faculty Opinions recommendation of Extracellular matrix stiffness and cell contractility control RNA localization to promote cell migration.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.731988381.793541516 ◽

2018 ◽

Author(s):

Martin A Schwartz

Keyword(s):

Extracellular Matrix ◽

Cell Migration ◽

Rna Localization ◽

Matrix Stiffness ◽

Cell Contractility ◽

Promote Cell Migration ◽

Extracellular Matrix Stiffness

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Enhanced Piezoelectric Fibered Extracellular Matrix to Promote Cardiomyocyte Maturation and Tissue Formation: A 3D Computational Model

Biology ◽

10.3390/biology10020135 ◽

2021 ◽

Vol 10 (2) ◽

pp. 135

Author(s):

Pau Urdeitx ◽

Mohamed H. Doweidar

Keyword(s):

Extracellular Matrix ◽

Cell Migration ◽

Computational Models ◽

Cell Junctions ◽

Tissue Formation ◽

Cardiac Muscle Cells ◽

Cell Processes ◽

Electrical Stimuli ◽

Cell Cell

Mechanical and electrical stimuli play a key role in tissue formation, guiding cell processes such as cell migration, differentiation, maturation, and apoptosis. Monitoring and controlling these stimuli on in vitro experiments is not straightforward due to the coupling of these different stimuli. In addition, active and reciprocal cell–cell and cell–extracellular matrix interactions are essential to be considered during formation of complex tissue such as myocardial tissue. In this sense, computational models can offer new perspectives and key information on the cell microenvironment. Thus, we present a new computational 3D model, based on the Finite Element Method, where a complex extracellular matrix with piezoelectric properties interacts with cardiac muscle cells during the first steps of tissue formation. This model includes collective behavior and cell processes such as cell migration, maturation, differentiation, proliferation, and apoptosis. The model has employed to study the initial stages of in vitro cardiac aggregate formation, considering cell–cell junctions, under different extracellular matrix configurations. Three different cases have been purposed to evaluate cell behavior in fibered, mechanically stimulated fibered, and mechanically stimulated piezoelectric fibered extra-cellular matrix. In this last case, the cells are guided by the coupling of mechanical and electrical stimuli. Accordingly, the obtained results show the formation of more elongated groups and enhancement in cell proliferation.

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Comparison of 10 murine models reveals a distinct biomechanical phenotype in thoracic aortic aneurysms

Journal of The Royal Society Interface ◽

10.1098/rsif.2016.1036 ◽

2017 ◽

Vol 14 (130) ◽

pp. 20161036 ◽

Cited By ~ 35

Author(s):

C. Bellini ◽

M. R. Bersi ◽

A. W. Caulk ◽

J. Ferruzzi ◽

D. M. Milewicz ◽

...

Keyword(s):

Extracellular Matrix ◽

Structural Integrity ◽

Ascending Aorta ◽

Elastic Fibre ◽

Cytoskeletal Proteins ◽

Aortic Aneurysms ◽

Genetic Mutations ◽

Murine Models ◽

Thoracic Aortic Aneurysms ◽

Signalling Molecules

Thoracic aortic aneurysms are life-threatening lesions that afflict young and old individuals alike. They frequently associate with genetic mutations and are characterized by reduced elastic fibre integrity, dysfunctional smooth muscle cells, improperly remodelled collagen and pooled mucoid material. There is a pressing need to understand better the compromised structural integrity of the aorta that results from these genetic mutations and renders the wall vulnerable to dilatation, dissection or rupture. In this paper, we compare the biaxial mechanical properties of the ascending aorta from 10 murine models: wild-type controls, acute elastase-treated, and eight models with genetic mutations affecting extracellular matrix proteins, transmembrane receptors, cytoskeletal proteins, or intracellular signalling molecules. Collectively, our data for these diverse mouse models suggest that reduced mechanical functionality, as indicated by a decreased elastic energy storage capability or reduced distensibility, does not predispose to aneurysms. Rather, despite normal or lower than normal circumferential and axial wall stresses, it appears that intramural cells in the ascending aorta of mice prone to aneurysms are unable to maintain or restore the intrinsic circumferential material stiffness, which may render the wall biomechanically vulnerable to continued dilatation and possible rupture. This finding is consistent with an underlying dysfunctional mechanosensing or mechanoregulation of the extracellular matrix, which normally endows the wall with both appropriate compliance and sufficient strength.

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Cellular dynamics of EMT: lessons from live in vivo imaging of embryonic development

Cell Communication and Signaling ◽

10.1186/s12964-021-00761-8 ◽

2021 ◽

Vol 19 (1) ◽

Author(s):

Jeffrey D. Amack

Keyword(s):

Extracellular Matrix ◽

Embryonic Development ◽

In Vivo Imaging ◽

Cytoskeletal Proteins ◽

Cell Junctions ◽

Model Organisms ◽

Cellular Dynamics ◽

Mesenchymal Transition ◽

Cell Cell

AbstractEpithelial-mesenchymal transition (EMT) refers to a process in which epithelial cells lose apical-basal polarity and loosen cell–cell junctions to take on mesenchymal cell morphologies and invasive properties that facilitate migration through extracellular matrix. EMT—and the reverse mesenchymal-epithelial transition (MET)—are evolutionarily conserved processes that are used throughout embryonic development to drive tissue morphogenesis. During adult life, EMT is activated to close wounds after injury, but also can be used by cancers to promote metastasis. EMT is controlled by several mechanisms that depend on context. In response to cell–cell signaling and/or interactions with the local environment, cells undergoing EMT make rapid changes in kinase and adaptor proteins, adhesion and extracellular matrix molecules, and gene expression. Many of these changes modulate localization, activity, or expression of cytoskeletal proteins that mediate cell shape changes and cell motility. Since cellular changes during EMT are highly dynamic and context-dependent, it is ideal to analyze this process in situ in living organisms. Embryonic development of model organisms is amenable to live time-lapse microscopy, which provides an opportunity to watch EMT as it happens. Here, with a focus on functions of the actin cytoskeleton, I review recent examples of how live in vivo imaging of embryonic development has led to new insights into mechanisms of EMT. At the same time, I highlight specific developmental processes in model embryos—gastrulation in fly and mouse embryos, and neural crest cell development in zebrafish and frog embryos—that provide in vivo platforms for visualizing cellular dynamics during EMT. In addition, I introduce Kupffer’s vesicle in the zebrafish embryo as a new model system to investigate EMT and MET. I discuss how these systems have provided insights into the dynamics of adherens junction remodeling, planar cell polarity signaling, cadherin functions, and cytoskeletal organization during EMT, which are not only important for understanding development, but also cancer progression. These findings shed light on mechanisms of actin cytoskeletal dynamics during EMT, and feature live in vivo imaging strategies that can be exploited in future work to identify new mechanisms of EMT and MET.

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Cell-extracellular matrix interactions under in vivo conditions during interstitial cell migration in Hydra vulgaris

Development ◽

10.1242/dev.120.2.425 ◽

1994 ◽

Vol 120 (2) ◽

pp. 425-432 ◽

Cited By ~ 2

Author(s):

X. Zhang ◽

M.P. Sarras

Keyword(s):

Extracellular Matrix ◽

Cell Migration ◽

Synthetic Peptide ◽

Interstitial Cell ◽

Extracellular Matrix Components ◽

Matrix Interactions ◽

Apical Half ◽

Matrix Components ◽

Extracellular Matrix Interactions

Interstitial cell (I-cell) migration in hydra is essential for establishment of the regional cell differentiation pattern in the organism. All previous in vivo studies have indicated that cell migration in hydra is a result of cell-cell interactions and chemotaxic gradients. Recently, in vitro cell adhesion studies indicated that isolated nematocytes could bind to substrata coated with isolated hydra mesoglea, fibronectin and type IV collagen. Under these conditions, nematocytes could be observed to migrate on some of these extracellular matrix components. By modifying previously described hydra grafting techniques, two procedures were developed to test specifically the role of extracellular matrix components during in vivo I-cell migration in hydra. In one approach, the extracellular matrix structure of the apical half of the hydra graft was perturbed using beta-aminopropionitrile and beta-xyloside. In the second approach, grafts were treated with fibronectin, RGDS synthetic peptide and antibody to fibronectin after grafting was performed. In both cases, I-cell migration from the basal half to the apical half of the grafts was quantitatively analyzed. Statistical analysis indicated that beta-aminopropionitrile, fibronectin, RGDS synthetic peptide and antibody to fibronectin all were inhibitory to I-cell migration as compared to their respective controls. beta-xyloside treatment had no effect on interstitial cell migration. These results indicate the potential importance of cell-extracellular matrix interactions during in vivo I-cell migration in hydra.

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