A computational study of amoeboid motility in 3D: the role of extracellular matrix geometry, cell deformability, and cell–matrix adhesion

2020 ◽  
Author(s):  
Eric J. Campbell ◽  
Prosenjit Bagchi
Keyword(s):  
Extracellular Matrix ◽  
Computational Study ◽  
Cell Deformability ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Amoeboid Motility ◽  
Cell Matrix Adhesion

scholarly journals Perturbing integrin function inhibits microtubule growth from centrosomes, spindle assembly, and cytokinesis

2006 ◽  
Vol 174 (4) ◽  
pp. 491-497 ◽  
Author(s):  
Carlos G. Reverte ◽  
Angela Benware ◽  
Christopher W. Jones ◽  
Susan E. LaFlamme
Keyword(s):  
Mitotic Spindle ◽  
Cell Types ◽  
Cellular Systems ◽  
Integrin Β1 ◽  
Dynamic Changes ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Microtubule Growth ◽  
Cell Matrix Adhesion

In many mammalian cell types, integrin-mediated cell-matrix adhesion is required for the G1–S transition of the cell cycle. As cells approach mitosis, a dramatic remodeling of their cytoskeleton accompanies dynamic changes in matrix adhesion, suggesting a mechanistic link. However, the role of integrins in cell division remains mostly unexplored. Using two cellular systems, we demonstrate that a point mutation in the β1 cytoplasmic domain (β1 tail) known to decrease integrin activity supports entry into mitosis but inhibits the assembly of a radial microtubule array focused at the centrosome during interphase, the formation of a bipolar spindle at mitosis and cytokinesis. These events are restored by externally activating the mutant integrin with specific antibodies. This is the first demonstration that the integrin β1 tail can regulate centrosome function, the assembly of the mitotic spindle, and cytokinesis.

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 Fibronectin Polymerization Regulates the Composition and Stability of Extracellular Matrix Fibrils and Cell-Matrix Adhesions

2002 ◽  
Vol 13 (10) ◽  
pp. 3546-3559 ◽  
Author(s):  
Jane Sottile ◽  
Denise C. Hocking
Keyword(s):  
Extracellular Matrix ◽  
Collagen I ◽  
Matrix Deposition ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Adhesion Sites ◽  
Fibronectin Matrix ◽  
Thrombospondin 1 ◽  
Fibronectin Deposition ◽  
Cell Matrix Adhesion

Remodeling of extracellular matrices occurs during development, wound healing, and in a variety of pathological processes including atherosclerosis, ischemic injury, and angiogenesis. Thus, identifying factors that control the balance between matrix deposition and degradation during tissue remodeling is essential for understanding mechanisms that regulate a variety of normal and pathological processes. Using fibronectin-null cells, we found that fibronectin polymerization into the extracellular matrix is required for the deposition of collagen-I and thrombospondin-1 and that the maintenance of extracellular matrix fibronectin fibrils requires the continual polymerization of a fibronectin matrix. Further, integrin ligation alone is not sufficient to maintain extracellular matrix fibronectin in the absence of fibronectin deposition. Our data also demonstrate that the retention of thrombospondin-1 and collagen I into fibrillar structures within the extracellular matrix depends on an intact fibronectin matrix. An intact fibronectin matrix is also critical for maintaining the composition of cell–matrix adhesion sites; in the absence of fibronectin and fibronectin polymerization, neither α5β1 integrin nor tensin localize to fibrillar cell–matrix adhesion sites. These data indicate that fibronectin polymerization is a critical regulator of extracellular matrix organization and stability. The ability of fibronectin polymerization to act as a switch that controls the organization and composition of the extracellular matrix and cell–matrix adhesion sites provides cells with a means of precisely controlling cell-extracellular matrix signaling events that regulate many aspects of cell behavior including cell proliferation, migration, and differentiation.

Focal nodular hyperplasia of the liver: Composition of the extracellular matrix and expression of cell-cell and cell-matrix adhesion molecules

1995 ◽  
Vol 26 (10) ◽  
pp. 1114-1125 ◽  
Author(s):  
Jean-yves Scoazec ◽  
Jean-françois Flejou ◽  
Antonia D'errico ◽  
Anne Couvelard ◽  
Renata Kozyraki ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Adhesion Molecules ◽  
Focal Nodular Hyperplasia ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Nodular Hyperplasia ◽  
Cell Matrix Adhesion ◽  
Cell Cell

Role of extracellular matrix in regulating embryonic epithelial-mesenchymal transition

2012 ◽  
Vol 3 (4) ◽  
pp. 333-344
Author(s):  
Francesca Zito
Keyword(s):  
Extracellular Matrix ◽  
Epithelial Mesenchymal Transition ◽  
Membrane Receptors ◽  
Mesenchymal Transition ◽  
Functional Studies ◽  
Cell Matrix ◽  
Fibrotic Diseases ◽  
Cell Matrix Adhesion ◽  
Specific Membrane

AbstractEmbryogenesis and morphogenesis are characterized by complex cell rearrangements and movements which require appropriate interactions of cells with the surrounding extracellular matrix (ECM) by means of specific membrane receptors. Interest in the identification and purification of ECM components, as well as in conducting functional studies of them, including their ligands and other molecules involved in cell-matrix adhesion, has intensified in recent years, increasing our knowledge of developmental machinery. Cellular movements play an important role during the epithelial-mesenchymal transition (EMT) events, which are key processes in normal embryogenesis as well as in pathological conditions, such as fibrotic diseases and cancer. Thus, to more fully understand mechanisms underlying the EMT process, and for better knowledge of the embryonic defects related to this process, it would be useful to study the substrates on which EMT cells move during embryo development. This review focuses on a few different embryonic systems, taking into account the cell migration that occurs during EMT and highlighting, in particular, studies describing the direct involvement of ECM molecules.

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