scholarly journals DISC1 regulates cell–cell adhesion, cell–matrix adhesion and neurite outgrowth

2010 ◽  
Vol 15 (8) ◽  
pp. 798-809 ◽  
Author(s):  
T Hattori ◽  
S Shimizu ◽  
Y Koyama ◽  
K Yamada ◽  
R Kuwahara ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Neurite Outgrowth ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion ◽  
Cell Cell

scholarly journals Cell-matrix adhesion and cell-cell adhesion differentially control basal myosin oscillation and Drosophila egg chamber elongation

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Xiang Qin ◽  
Byung Ouk Park ◽  
Jiaying Liu ◽  
Bing Chen ◽  
Valerie Choesmel-Cadamuro ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Egg Chamber ◽  
Cell Matrix Adhesion ◽  
Cell Cell

Regulation of cell???matrix adhesion and potentially also cell???cell adhesion by MIA

2006 ◽  
Vol 16 (Supplement 1) ◽  
pp. S18-S19
Author(s):  
A. Winklmeier ◽  
R. Bauer ◽  
S. Arndt ◽  
A. Bosserhoff
Keyword(s):  
Cell Adhesion ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion ◽  
Cell Cell

DISC1 regulates cell–cell, cell–matrix adhesion and neurite outgrowth

2009 ◽  
Vol 65 ◽  
pp. S121
Author(s):  
Tsuyoshi Hattori ◽  
Syoko Shimizu ◽  
Kohei Yamada ◽  
Ryusuke Kuwahara ◽  
Kouji Oono ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion ◽  
Cell Cell

MATHEMATICAL MODELLING OF CANCER INVASION: THE IMPORTANCE OF CELL–CELL ADHESION AND CELL–MATRIX ADHESION

2011 ◽  
Vol 21 (04) ◽  
pp. 719-743 ◽  
Author(s):  
MARK A. J. CHAPLAIN ◽  
MIROSŁAW LACHOWICZ ◽  
ZUZANNA SZYMAŃSKA ◽  
DARIUSZ WRZOSEK
Keyword(s):  
Extracellular Matrix ◽  
Cell Adhesion ◽  
Cancer Cells ◽  
Classical Solutions ◽  
Invasion Process ◽  
Open Problems ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion ◽  
Cell Cell

The process of invasion of tissue by cancer cells is crucial for metastasis — the formation of secondary tumours — which is the main cause of mortality in patients with cancer. In the invasion process itself, adhesion, both cell–cell and cell–matrix, plays an extremely important role. In this paper, a mathematical model of cancer cell invasion of the extracellular matrix is developed by incorporating cell–cell adhesion as well as cell–matrix adhesion into the model. Considering the interactions between cancer cells, extracellular matrix and matrix degrading enzymes, the model consists of a system of reaction–diffusion partial integro–differential equations, with nonlocal (integral) terms describing the adhesive interactions between cancer cells and the host tissue, i.e. cell–cell adhesion and cell–matrix adhesion. Having formulated the model, we prove the existence and uniqueness of global in time classical solutions which are uniformly bounded. Then, using computational simulations, we investigate the effects of the relative importance of cell–cell adhesion and cell–matrix adhesion on the invasion process. In particular, we examine the roles of cell–cell adhesion and cell–matrix adhesion in generating heterogeneous spatio-temporal solutions. Finally, in the discussion section, concluding remarks are made and open problems are indicated.

scholarly journals Rap1GAP impairs cell-matrix adhesion in the absence of effects on cell-cell adhesion

2011 ◽  
Vol 5 (4) ◽  
pp. 323-331 ◽  
Author(s):  
Lisa A. Vuchak ◽  
Oxana M. Tsygankova ◽  
Judy L. Meinkoth
Keyword(s):  
Cell Adhesion ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion ◽  
Cell Cell

Differential effects of histamine and thrombin on endothelial barrier function through actin-myosin tension

2002 ◽  
Vol 282 (1) ◽  
pp. H21-H29 ◽  
Author(s):  
Alan B. Moy ◽  
Ken Blackwell ◽  
Anant Kamath
Keyword(s):  
Cell Adhesion ◽  
Barrier Function ◽  
Umbilical Vein ◽  
Collagen Membrane ◽  
Tension Development ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Adhesion Sites ◽  
Cell Matrix Adhesion ◽  
Cell Cell

We compared temporal changes in isometric tension in cultured human umbilical vein endothelial cells inoculated on a polymerized collagen membrane with changes in cell-cell and cell-matrix adhesion derived by a mathematical model of transendothelial cell resistance. Thrombin and histamine disrupt barrier function by targeting a greater loss in cell-cell adhesion, which preceded losses in overall transendothelial resistance. There were minor losses in cell-matrix adhesion, which was temporally slower than the decline in the overall transendothelial resistance. In contrast, thrombin and histamine restored barrier function by initiating a restoration of cell-matrix adhesion, which occurred before an increase in overall transendothelial resistance. Thrombin mediated a second and slower decline in cell-cell adhesion, which was not observed in histamine-treated cells. This decline in cell-cell adhesion temporally correlated with expressed maximal levels of tension development, suggesting that actin-myosin contraction directly strains cell-cell adhesion sites. Pretreatment of cells with ML-7 mediated more rapid recovery of cell-cell adhesion and had no effect on cell-matrix adhesion. Taken together, expression of actin-myosin contraction affects the restoration of barrier function by straining cell-cell adhesion sites.

scholarly journals RAP1-RAC1 Signaling Has an Important Role in Adhesion and Migration in HNSCC

2020 ◽  
Vol 99 (8) ◽  
pp. 959-968 ◽  
Author(s):  
M. Liu ◽  
R. Banerjee ◽  
C. Rossa ◽  
N.J. D’Silva
Keyword(s):  
Cell Migration ◽  
Cell Adhesion ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
And Migration ◽  
Rap1 Activation ◽  
Cell Matrix Adhesion ◽  
Α5β1 Integrin ◽  
Hnscc Cell ◽  
Cell Cell

Cell-cell adhesion is a key mechanism to control tissue integrity and migration. In head and neck squamous cell carcinoma (HNSCC), cell migration facilitates distant metastases and is correlated with poor prognosis. RAP1, a ras-like protein, has an important role in the progression of HNSCC. RAC1 is an integrin-linked, ras-like protein that promotes cell migration. Here we show that loss of cell-cell adhesion is correlated with inactivation of RAP1 confirmed by 2 different biochemical approaches. RAP1 activation is required for cell-matrix adhesion confirmed by adhesion to fibronectin-coated plates with cells that have biochemically activated RAP1. This effect is reversed when RAP1 is inactivated. In addition, RAP1GTP-mediated adhesion is only facilitated through α5β1 integrin complex and is not a function of either α5 or β1 integrin alone. Moreover, the inside-out signaling of RAP1 activation is coordinated with RAC1 activation. These findings show that RAP1 has a prominent role in cell-matrix adhesion via extracellular matrix molecule fibronectin-induced α5β1 integrin and supports a critical role for the RAP1/RAC1 signaling axis in HNSCC cell migration.

scholarly journals Epithelial Morphogenesis Driven by Cell-Matrix vs. Cell-Cell Adhesion

2020 ◽  
Author(s):  
Shaohe Wang ◽  
Kazue Matsumoto ◽  
Kenneth M. Yamada
Keyword(s):  
Cell Adhesion ◽  
Single Cell ◽  
Cell Sheet ◽  
Branching Morphogenesis ◽  
Epithelial Morphogenesis ◽  
Epithelial Surface ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion ◽  
Cell Cell

SUMMARYMany embryonic organs undergo epithelial morphogenesis to form tree-like hierarchical structures. However, it remains unclear what drives the budding and branching of stratified epithelia, such as in embryonic salivary gland and pancreas. Here, we performed live-organ imaging of mouse embryonic salivary glands at single-cell resolution to reveal that budding morphogenesis is driven by expansion and folding of a distinct epithelial surface cell sheet characterized by strong cell-matrix adhesions and weak cell-cell adhesions. Profiling of single-cell transcriptomes of this epithelium revealed spatial patterns of transcription underlying these cell adhesion differences. We then synthetically reconstituted budding morphogenesis by experimentally suppressing E-cadherin expression and inducing basement membrane formation in 3D spheroid cultures of engineered cells, which required β1 integrin-mediated cell-matrix adhesion for successful budding. Thus, stratified epithelial budding, the key first step of branching morphogenesis, is driven by an overall combination of strong cell-matrix adhesion and weak cell-cell adhesion by peripheral epithelial cells.

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.

Ezrin regulates cell-cell and cell-matrix adhesion, a possible role with E-cadherin/beta-catenin

1999 ◽  
Vol 112 (18) ◽  
pp. 3081-3090 ◽  
Author(s):  
S. Hiscox ◽  
W.G. Jiang
Keyword(s):  
Cancer Cells ◽  
Focal Adhesions ◽  
Beta Catenin ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Ezrin Expression ◽  
Coated Surfaces ◽  
Cell Matrix Adhesion ◽  
E Cadherin ◽  
Cell Cell

Ezrin, radixin, moesin and merlin form a subfamily of conserved proteins in the band 4.1 superfamily. The function of these proteins is to link the plasma membrane to the actin cytoskeleton. Merlin is defective or absent in schwannomas and meningiomas and has been suggested to function as a tumour suppressor. In this study, we have examined the role of ezrin as a potential regulator of the adhesive and invasive behaviour of tumour cells. We have shown that following inhibition of ezrin expression in colo-rectal cancer cells using antisense oligonucleotides, these cells displayed a reduced cell-cell adhesiveness together with a gain in their motile and invasive behaviour. These cells also displayed increased spreading over matrix-coated surfaces. Immunofluorescence studies revealed that antisense-treated cells also displayed an increased staining of paxillin in areas representing focal adhesions. Furthermore, coprecipitation studies revealed an association of ezrin with E-cadherin and beta-catenin. Induction of the phosphorylation of ezrin by orthovanadate and hepatocyte growth factor/scatter factor resulted in changes similar to those seen with antisense treatment, together with a marked decrease in the association of ezrin with both beta-catenin and E-cadherin. It is concluded that ezrin regulates cell-cell and cell-matrix adhesion, by interacting with cell adhesion molecules E-cadherin and beta-catenin, and may thus play an important role in the control of adhesion and invasiveness of cancer cells.

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