scholarly journals Micropatterned Multicolor Dynamically Adhesive Substrates to Control Cell Adhesion and Multicellular Organization

Langmuir ◽  
2014 ◽  
Vol 30 (5) ◽  
pp. 1327-1335 ◽  
Author(s):  
Natalia M. Rodriguez ◽  
Ravi A. Desai ◽  
Britta Trappmann ◽  
Brendon M. Baker ◽  
Christopher S. Chen
Keyword(s):  
Cell Adhesion ◽  
Control Cell

Development of Polymer/Nanodiamond Composite Coatings to Control Cell Adhesion, Growth, and Functions

2015 ◽  
pp. 1-26 ◽  
Author(s):  
Milena Keremidarska ◽  
Kamelia Hristova ◽  
Todor Hikov ◽  
Ekaterina Radeva ◽  
Dimitar Mitev ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Composite Coatings ◽  
Control Cell

scholarly journals Interconnected Microchannels in Hydrogels to Control Cell Adhesion and Mechanotransduction

2018 ◽  
Vol 114 (3) ◽  
pp. 192a
Author(s):  
Mohammadreza Taale ◽  
Christine Arndt ◽  
Christine Selhuber-Unkel
Keyword(s):  
Cell Adhesion ◽  
Control Cell

Molding Micropatterns of Elasticity on PEG-Based Hydrogels to Control Cell Adhesion and Migration

2011 ◽  
Vol 13 (10) ◽  
pp. B395-B404 ◽  
Author(s):  
Mar Diez ◽  
Vera A. Schulte ◽  
Filippo Stefanoni ◽  
Carlo F. Natale ◽  
Francesco Mollica ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Control Cell ◽  
Cell Adhesion And Migration ◽  
And Migration

scholarly journals Light-Modulated Cell Adhesion to Control Cell and Tissue Morphogenesis

2014 ◽  
Vol 106 (2) ◽  
pp. 789a
Author(s):  
Jeffrey van Haren ◽  
Torsten Wittmann
Keyword(s):  
Cell Adhesion ◽  
Control Cell ◽  
Tissue Morphogenesis

scholarly journals Mechano-redox control of integrin de-adhesion

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Freda Passam ◽  
Joyce Chiu ◽  
Lining Ju ◽  
Aster Pijning ◽  
Zeenat Jahan ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Ligand Binding ◽  
Protein Interactions ◽  
Metal Binding ◽  
Control Function ◽  
Control Cell ◽  
Mechanical Force ◽  
Cell Surface Receptor ◽  
Adhesive Properties ◽  
Αiibβ3 Integrin

How proteins harness mechanical force to control function is a significant biological question. Here we describe a human cell surface receptor that couples ligand binding and force to trigger a chemical event which controls the adhesive properties of the receptor. Our studies of the secreted platelet oxidoreductase, ERp5, have revealed that it mediates release of fibrinogen from activated platelet αIIbβ3 integrin. Protein chemical studies show that ligand binding to extended αIIbβ3 integrin renders the βI-domain Cys177-Cys184 disulfide bond cleavable by ERp5. Fluid shear and force spectroscopy assays indicate that disulfide cleavage is enhanced by mechanical force. Cell adhesion assays and molecular dynamics simulations demonstrate that cleavage of the disulfide induces long-range allosteric effects within the βI-domain, mainly affecting the metal-binding sites, that results in release of fibrinogen. This coupling of ligand binding, force and redox events to control cell adhesion may be employed to regulate other protein-protein interactions.

scholarly journals PS2 - 167 CIC Deficiency is Associated with Dysregulation of Genes Involved in Cell Adhesion and Developmental Processes

2016 ◽  
Vol 43 (S4) ◽  
pp. S13-S13
Author(s):  
V.G. LeBlanc ◽  
S. Chittaranjan ◽  
M. Firme ◽  
S.Y. Chan ◽  
J. Song ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Cell Lines ◽  
Somatic Mutations ◽  
Control Cell ◽  
The Cancer Genome Atlas ◽  
Mitogen Activated Protein Kinase ◽  
Low Grade ◽  
Type I ◽  
Developmental Processes

Somatic mutations in the Capicua (CIC) gene were first identified in Type I low-grade gliomas (LGGs), which are characterized by 1p/19q co-deletions and IDH mutations. They are found at frequencies of ~50-70% in this glioma subtype, and have since been identified in ~40% of stomach adenocarcinomas (STADs) of the microsatellite instability (MSI) subtype; however, the role of these somatic mutations in malignancy has yet to be established. In Drosophila, CIC functions as a transcriptional repressor whose activity is inhibited upon activation of the mitogen-activated protein kinase (MAPK) signalling pathway. Though mammalian CIC appears to retain these functions, only three of its target genes have been established in human cells: ETV1, ETV4, and ETV5 (ETV1/4/5). To further probe CIC’s transcriptional network, we developed CIC knockout cell lines and performed transcriptomic and proteiomic analyses in these and in control cell lines expressing wild type CIC, identifying a total of 582 differentially expressed genes. We also used RNA-seq data from The Cancer Genome Atlas (TCGA) for Type I LGGs and STADs to perform additional differential expression analyses between CIC-deficient and CIC-expressing samples. Though gene-level overlap was limited between the three contexts, we found that CIC appears to regulate the expression of genes involved in cell-cell adhesion, metabolism, and developmental processes in all three contexts. These results shed light on the pathological role of CIC mutations and may help explain why these have been associated with poorer outcome within Type I LGGs.

scholarly journals Bioactive Magnetoelastic Materials as Coatings for Implantable Biomaterials

2009 ◽  
Vol 3 (2) ◽  
Author(s):  
E. Vlaisavljevich ◽  
L. Janka ◽  
K. Ong ◽  
R. Rajachar
Keyword(s):  
Cell Adhesion ◽  
Soft Tissue ◽  
Cell Viability ◽  
Control Cell ◽  
Fibrous Tissue ◽  
Fluorescent Imaging ◽  
Biomedical Implants ◽  
Stability Function ◽  
Tissue Interface ◽  
The Stability

Enhanced fibroblast activity at the soft tissue-implant interface can dramatically decrease the stability, function, and lifespan of biomedical implants such as bone anchored prostheses. Although bone anchoring systems dramatically improve prosthetic limb mechanical stability, uncontrolled fibrosis at the soft tissue-mounting post interface is a significant problem. The aberrant cell growth leads to irregular skin folds that prevent proper sealing to the bone anchoring post and also serves as a site for opportunistic infection and failure of the prosthetic system. We are developing a bioactive vibrational coating to control fibrous tissue overgrowth. The coating is based on a magnetoelastic (ME) material that can be set to vibrate at a predetermined amplitude and frequency using a controlled magnetic field. We hypothesize that small local vibrations can be used to selectively control cell adhesion and gene expression to promote and maintain functional stability at the implant-tissue interface. For bone anchored prostheses, the ME coating would be applied around the mounting post at the soft tissue interface. The specific aims of this work were to (1) modify the coating for use in contact with a biologic environment and (2) determine if local vibrational strain can efficiently control cell attachment to the coating without significantly influencing viability. First, two common biocompatible polymers, polyurethane and chitosan, were deposited as thin films on the ME coating to allow for its use in tissue culture. An indirect cytotoxicity test was used to determine fibroblast (L929) viability in media conditioned for 24 and 48 hours with uncoated, chitosan coated, and polyurethane coated ME materials. Results demonstrated that both polymer coatings returned cell survival to levels statistically indistinguishable from controls (cells cultured on tissue cultured polystyrene, TCP) with cell viability over 96% under all coating conditions. Second, the affect of local vibrations on cell adhesion was tested in vitro. A cell viability assay (Calcein-AM) followed by fluorescent imaging was used to quantify attachment and viability of fibroblasts cultured directly on the bioactive ME material. Results clearly indicated that controlled local vibrations can induce complete cell detachment from the ME material compared with non-vibrated controls at up to 72 hours post-seeding. Further, cells detached via applied vibrations showed no significant decrease in viability compared to adherent controls. These results suggest the potential for this novel coating to effectively control fibrous tissue overgrowth using the mild application of tunable local vibrations, a significant and cost-effective approach that could improve the stability, function, and lifespan of biomedical implants and reduce the need for surgical revision.

scholarly journals The CEACAM1-L Glycoprotein Associates with the Actin Cytoskeleton and Localizes to Cell–Cell Contact through Activation of Rho-like GTPases

2000 ◽  
Vol 11 (1) ◽  
pp. 65-77 ◽  
Author(s):  
Svetlana Sadekova ◽  
Nathalie Lamarche-Vane ◽  
Xiaodong Li ◽  
Nicole Beauchemin
Keyword(s):  
Cell Adhesion ◽  
Actin Cytoskeleton ◽  
Adhesion Molecule ◽  
Control Cell ◽  
Growth Inhibitor ◽  
Cytoplasmic Domain ◽  
Cell Contact ◽  
A Cell ◽  
Rho Family ◽  
Cell Cell

Associations between plasma membrane-linked proteins and the actin cytoskeleton play a crucial role in defining cell shape and determination, ensuring cell motility and facilitating cell–cell or cell–substratum adhesion. Here, we present evidence that CEACAM1-L, a cell adhesion molecule of the carcinoembryonic antigen family, is associated with the actin cytoskeleton. We have delineated the regions involved in actin cytoskeleton association to the distal end of the CEACAM1-L long cytoplasmic domain. We have demonstrated that CEACAM1-S, an isoform of CEACAM1 with a truncated cytoplasmic domain, does not interact with the actin cytoskeleton. In addition, a major difference in subcellular localization of the two CEACAM1 isoforms was observed. Furthermore, we have established that the localization of CEACAM1-L at cell–cell boundaries is regulated by the Rho family of GTPases. The retention of the protein at the sites of intercellular contacts critically depends on homophilic CEACAM1–CEACAM1 interactions and association with the actin cytoskeleton. Our results provide new evidence on how the Rho family of GTPases can control cell adhesion: by directing an adhesion molecule to its proper cellular destination. In addition, these results provide an insight into the mechanisms of why CEACAM1-L, but not CEACAM1-S, functions as a tumor cell growth inhibitor.

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