Modeling Cell-Cell Adhesion With a Cadherin Based Model

2012 ◽  
Author(s):  
John Dallon
Keyword(s):  
Wound Healing ◽  
Cell Adhesion ◽  
Tissue Formation ◽  
Adhesion Sites ◽  
Actin Structure ◽  
Cell Cell

Cell-cell adhesion is critical in morphogenesis, tissue formation, cancer, and wound healing. A better understanding of cell-cell adhesion mediated by cadherins will allow all these processes to be mimicked and manipulated to achieve desired objectives. This paper investigates the role of the actin structure associated with cadherin adhesion sites.

Abstract 361: Creg1 Interacts With Sec8 to Promote Cell-cell Adhesion During Cardiomyogenesis

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Jie Liu ◽  
Yanmei Qi ◽  
Shu-Chan Hsu ◽  
Siavash Saadat ◽  
Saum Rahimi ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Es Cells ◽  
Embryonic Stem ◽  
Intercellular Junctions ◽  
Amino Acid Residues ◽  
Loss Of Function ◽  
Wild Type ◽  
Adhesion Sites ◽  
Cell Cell

Cellular repressor of E1A-stimulated genes 1 (CREG1) is a 24 kD glycoprotein essential for early embryonic development. Our immunofluorescence studies revealed that CREG1 is highly expressed at myocyte junctions in both embryonic and adult hearts. To explore it role in cardiomyogenesis, we employed gain- and loss-of-function analyses demonstrating that CREG1 is required for the differentiation of mouse embryonic stem (ES) cell into cohesive myocardium-like structures. Chimeric cultures of wild-type and CREG1 knockout ES cells expressing cardiac-specific reporters showed that the cardiomyogenic effect of CREG1 is cell autonomous. Furthermore, we identified a novel interaction between CREG1 and Sec8 of the exocyst complex, which tethers vesicles to the plasma membrane. Mutations of the amino acid residues D141 and P142 to alanine in CREG1 abolished its binding to Sec8. To address the role of the CREG1-Sec8 interaction in cardiomyogenesis, we rescued CREG1 knockout ES cells with wild-type and Sec8-binding mutant CREG1 and showed that CREG1 binding to Sec8 promotes cardiomyocyte differentiation and cohesion. Mechanistically, CREG1, Sec8 and N-cadherin all localize at cell-cell adhesion sites. CREG1 overexpression enhances the assembly of adherens and gap junctions. By contrast, its knockout inhibits the Sec8-N-cadherin interaction and induces their degradation. Finally, shRNA-mediated knockdown of Sec8 leads to cardiomyogenic defects similar to CREG1 knockout. These results suggest that the CREG1 binding to Sec8 enhances the assembly of intercellular junctions and promotes cardiomyogenesis.

scholarly journals The Role of Cell-Cell Adhesion in Wound Healing

2006 ◽  
Vol 128 (1-2) ◽  
pp. 209-218 ◽  
Author(s):  
Evgeniy Khain ◽  
Leonard M. Sander ◽  
Casey M. Schneider-Mizell
Keyword(s):  
Wound Healing ◽  
Cell Adhesion ◽  
Cell Cell

scholarly journals Novel role of nectin: implication in the co-localization of JAM-A and claudin-1 at the same cell-cell adhesion membrane domain

2008 ◽  
Vol 13 (8) ◽  
pp. 797-805 ◽  
Author(s):  
Kaori Kuramitsu ◽  
Wataru Ikeda ◽  
Naoya Inoue ◽  
Yoshiyuki Tamaru ◽  
Yoshimi Takai
Keyword(s):  
Cell Adhesion ◽  
Membrane Domain ◽  
Cell Cell

scholarly journals Combining experiments and in silico modeling to infer the role of adhesion and proliferation on the collective dynamics of cells

2021 ◽  
Author(s):  
Hygor P. M. Melo ◽  
F. Raquel Maia ◽  
André S. Nunes ◽  
Rui L. Reis ◽  
Joaquim M. Oliveira ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Cell Adhesion ◽  
Glioblastoma Multiforme ◽  
In Silico ◽  
Relative Importance ◽  
Collective Dynamics ◽  
Surfaces And Interfaces ◽  
In Silico Modeling ◽  
Cell Cell

ABSTRACTThe collective dynamics of cells on surfaces and interfaces poses technological and theoretical challenges in the study of morphogenesis, tissue engineering, and cancer. Different mechanisms are at play, including, cell-cell adhesion, cell motility, and proliferation. However, the relative importance of each one is elusive. Here, experiments with a culture of glioblastoma multiforme cells on a substrate are combined with in silico modeling to infer the rate of each mechanism. By parametrizing these rates, the time-dependence of the spatial correlation observed experimentally is reproduced. The obtained results suggest a reduction in cell-cell adhesion with the density of cells. The reason for such reduction and possible implications for the collective dynamics of cancer cells are discussed.

Role of the second immunoglobulin-like loop of nectin in cell–cell adhesion

2002 ◽  
Vol 293 (1) ◽  
pp. 45-49 ◽  
Author(s):  
Yumiko Momose ◽  
Tomoyuki Honda ◽  
Maiko Inagaki ◽  
Kazuya Shimizu ◽  
Kenji Irie ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Cell Cell

Expression and role of E- and P-cadherin adhesion molecules in embryonic histogenesis. I. Lung epithelial morphogenesis

Development ◽  
1989 ◽  
Vol 105 (2) ◽  
pp. 263-270 ◽  
Author(s):  
Y. Hirai ◽  
A. Nose ◽  
S. Kobayashi ◽  
M. Takeichi
Keyword(s):  
Monoclonal Antibody ◽  
Cell Adhesion ◽  
Epithelial Cells ◽  
Adhesion Molecules ◽  
Lung Epithelial Cells ◽  
Early Developmental Stage ◽  
Subtle Effect ◽  
Lung Epithelial ◽  
Cell Cell

The role of Ca2+-dependent cell-cell adhesion molecules, E- and P-cadherins, in the histogenesis of mouse embryonic lung was studied. All epithelial cells of the lung express both E- and P-cadherin at the early developmental stage. P-cadherin, however, gradually disappears during development, initially from the main bronchi and eventually from all epithelial cells. When a monoclonal antibody to E-cadherin (ECCD-1) was added to monolayer cultures of lung epithelial cells, it induced a partial disruption of their cell-cell adhesion, while a monoclonal antibody to P-cadherin (PCD-1) showed a subtle effect. A mixture of the two antibodies, however, displayed a synergistic effect. We then tested the effect of the antibodies on the morphogenesis of lung primordia using an organ culture system. In control media, the explants formed typical bronchial trees. In the presence of ECCD-1, the explants grew up at the same rate as in the control, but their morphogenesis was affected. The control explants formed round epithelial lobules with an open luminal space at the tips of the bronchial trees, whereas the lobules of explants incubated with ECCD-1 tended to be flat and devoid of the luminal space. PCD-1 showed a similar but very small effect. A mixture of the two antibodies, however, showed a stronger effect: the branching of epithelia was partially suppressed and the arrangement of epithelial cells was distorted in many places. These results suggest that E- and P-cadherin have a synergistic role in the organization of epithelial cells in lung morphogenesis.

E-cadherin mediated cell adhesion recruits SAP97 into the cortical cytoskeleton

1998 ◽  
Vol 111 (8) ◽  
pp. 1071-1080 ◽  
Author(s):  
S.M. Reuver ◽  
C.C. Garner
Keyword(s):  
Cell Adhesion ◽  
Model Systems ◽  
Molecular Organization ◽  
Cell Contact ◽  
Adhesion Sites ◽  
Associated Proteins ◽  
Adhesion Complex ◽  
Cortical Cytoskeleton ◽  
E Cadherin ◽  
Cell Cell

Members of the SAP family of synapse-associated proteins have recently emerged as central players in the molecular organization of synapses. In this study, we have examined the mechanism that localizes one member, SAP97, to sites of cell-cell contact. Utilizing epithelial CACO-2 cells and fibroblast L-cells as model systems, we demonstrate that SAP97 is associated with the submembranous cortical cytoskeleton at cell-cell adhesion sites. Furthermore, we show that its localization into this structure is triggered by E-cadherin. Although SAP97 can be found in an E-cadherin/catenin adhesion complex, this interaction seems to be mediated by the attachment of SAP97 to the cortical cytoskeleton. Our results are consistent with a model in which SAP97 is recruited to sites of cell-cell contact via an E-cadherin induced assembly of the cortical cytoskeleton.

scholarly journals The Role of MicroRNAs in Epidermal Barrier

2020 ◽  
Vol 21 (16) ◽  
pp. 5781
Author(s):  
Ai-Young Lee
Keyword(s):  
Cell Adhesion ◽  
Critical Role ◽  
Keratinocyte Differentiation ◽  
Epidermal Barrier ◽  
Barrier Integrity ◽  
Skin Lipids ◽  
Differentiation And Proliferation ◽  
The Impact ◽  
Cell Cell

MicroRNAs (miRNAs), which mostly cause target gene silencing via transcriptional repression and degradation of target mRNAs, regulate a plethora of cellular activities, such as cell growth, differentiation, development, and apoptosis. In the case of skin keratinocytes, the role of miRNA in epidermal barrier integrity has been identified. Based on the impact of key genetic and environmental factors on the integrity and maintenance of skin barrier, the association of miRNAs within epidermal cell differentiation and proliferation, cell–cell adhesion, and skin lipids is reviewed. The critical role of miRNAs in the epidermal barrier extends the use of miRNAs for control of relevant skin diseases such as atopic dermatitis, ichthyoses, and psoriasis via miRNA-based technologies. Most of the relevant miRNAs have been associated with keratinocyte differentiation and proliferation. Few studies have investigated the association of miRNAs with structural proteins of corneocytes and cornified envelopes, cell–cell adhesion, and skin lipids. Further studies investigating the association between regulatory and structural components of epidermal barrier and miRNAs are needed to elucidate the role of miRNAs in epidermal barrier integrity and their clinical implications.

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