scholarly journals Vaccinia Virus Induces Ca2+-Independent Cell-Matrix Adhesion during the Motile Phase of Infection

1998 ◽  
Vol 72 (12) ◽  
pp. 9924-9933 ◽  
Author(s):  
Christopher M. Sanderson ◽  
Geoffrey L. Smith
Keyword(s):  
Vaccinia Virus ◽  
Cell Motility ◽  
Viral Gene Expression ◽  
Viral Gene ◽  
Fibronectin Receptor ◽  
Culture Flask ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Infected Cells ◽  
Cell Matrix Adhesion

ABSTRACT Vaccinia virus (VV) induces two forms of cell motility: cell migration, which is dependent on the expression of early genes, and the formation of cellular projections, which requires the expression of late genes. The need for viral gene expression prior to cell motility suggests that VV proteins may affect how infected cells interact with the extracellular matrix. To address this, we have analyzed changes in cell-matrix adhesion after infection of BS-C-1 cells with VV. Whereas uninfected cells round up and detach from the culture flask in the presence of EGTA, infected cells remain attached to the culture flask with a stellate morphology. Ca2+-independent cell-matrix adhesion was evident by 10 h postinfection, after the onset of cell motility but before the formation of virus-induced cellular projections. Progression to Ca2+-independent adhesion required the expression of late viral genes but not the formation of intracellular enveloped virus particles or intracellular actin tails. Analyses of specific matrix proteins identified vitronectin and fibronectin as optimal ligands for Ca2+-independent adhesion and the formation of cellular projections. Adhesion to fibronectin was mediated via RGD motifs alone and was not inhibited by 500 μg of heparin/ml. Kistrin, a disintegrin which binds preferentially to the αvβ3 (vitronectin/fibronectin) receptor inhibited the formation of cellular projections without disrupting preformed matrix interactions. Finally, we show that Ca2+-independent cell-matrix adhesion is a dynamic process which mediates changes in the morphology of VV-infected cells and uninfected cells which exhibit a transformed phenotype.

scholarly journals The MIG-2/Integrin Interaction Strengthens Cell-Matrix Adhesion and Modulates Cell Motility

2007 ◽  
Vol 282 (28) ◽  
pp. 20455-20466 ◽  
Author(s):  
Xiaohua Shi ◽  
Yan-Qing Ma ◽  
Yizeng Tu ◽  
Ka Chen ◽  
Shan Wu ◽  
...  
Keyword(s):  
Cell Motility ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion

scholarly journals Computational modelling of cell motility modes emerging from cell-matrix adhesion dynamics

2021 ◽  
Author(s):  
Leonie van Steijn ◽  
Clément Sire ◽  
Loïc Dupré ◽  
Guy Theraulaz ◽  
Roeland M.H. Merks
Keyword(s):  
Random Walks ◽  
Cell Motility ◽  
Adhesion Formation ◽  
Computational Modelling ◽  
Target Cells ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Lévy Walks ◽  
Cell Matrix Adhesion

Lymphocytes have been described to perform different motility patterns such as Brownian random walks, persistent random walks, and Lévy walks. Depending on the conditions, such as confinement or the distribution of target cells, either Brownian or Lévy walks lead to more efficient interaction with the targets. The diversity of these motility patterns may be explained by an adaptive response to the surrounding extracellular matrix (ECM). Indeed, depending on the ECM composition, lymphocytes either display a floating motion without attaching to the ECM, or sliding and stepping motion with respectively continuous or discontinuous attachment to the ECM, or pivoting behaviour with sustained attachment to the ECM. Moreover, on the long term, lymphocytes either perform a persistent random walk or a Brownian-like movement depending on the ECM composition. How the ECM affects cell motility is still incompletely understood. Here, we integrate essential mechanistic details of the lymphocyte-matrix adhesions and lymphocyte intrinsic cytoskeletal induced cell propulsion into a Cellular Potts model (CPM). We show that the combination of \textit{de novo} cell-matrix adhesion formation, adhesion growth and shrinkage, adhesion rupture, and feedback of adhesions onto cell propulsion recapitulates multiple lymphocyte behaviours, for different lymphocyte subsets and various substrates. With an increasing attachment area and increased adhesion strength, the cells' speed and persistence decreases. Additionally, the model can predict short-term persistent with long-term subdiffusive motility, showing a pivoting motion. For small adhesion areas, we observe that the spatial distribution of adhesions influences cell motility. Small adhesions at the front allow for more persistent motion than larger clusters at the back, despite a similar total adhesion area. In conclusion, we present an integrated framework to simulate the effects of ECM proteins on cell-matrix adhesion dynamics. The model reveals a sufficient set of principles explaining the plasticity of lymphocyte motility.

scholarly journals Alpha Actinin-1 Regulates Cell-Matrix Adhesion Organization in Keratinocytes: Consequences for Skin Cell Motility

2015 ◽  
Vol 135 (4) ◽  
pp. 1043-1052 ◽  
Author(s):  
Kevin J. Hamill ◽  
Sho Hiroyasu ◽  
Zachary T. Colburn ◽  
Rosa V. Ventrella ◽  
Susan B. Hopkinson ◽  
...  
Keyword(s):  
Cell Motility ◽  
Matrix Adhesion ◽  
Skin Cell ◽  
Cell Matrix ◽  
Cell Matrix Adhesion

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.

scholarly journals Cell–matrix adhesion

2007 ◽  
Vol 213 (3) ◽  
pp. 565-573 ◽  
Author(s):  
Allison L. Berrier ◽  
Kenneth M. Yamada
Keyword(s):  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion

scholarly journals Patterns of accumulation of miRNAs encoded by herpes simplex virus during productive infection, latency, and on reactivation

2014 ◽  
Vol 112 (1) ◽  
pp. E49-E55 ◽  
Author(s):  
Te Du ◽  
Zhiyuan Han ◽  
Guoying Zhou ◽  
Bernard Roizman
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Cultured Cells ◽  
Viral Gene Expression ◽  
The Body ◽  
Productive Infection ◽  
Viral Gene ◽  
Infected Cells ◽  
Simplex Virus ◽  
Portal Of Entry

The key events in herpes simplex virus (HSV) infections are (i) replication at a portal of entry into the body modeled by infection of cultured cells; (ii) establishment of a latent state characterized by a sole latency-associated transcript and microRNAs (miRNAs) modeled in murine peripheral ganglia 30 d after inoculation; and (iii) reactivation from the latent state modeled by excision and incubation of ganglia in medium containing anti-NGF antibody for a timespan of a single viral replicative cycle. In this report, we examine the pattern of synthesis and accumulation of 18 HSV-1 miRNAs in the three models. We report the following: (i) H2-3P, H3-3P, H4-3P, H5-3P, H6-3P, and H7-5P accumulated in ganglia harboring latent virus. All but H4-3P were readily detected in productively infected cells, and most likely they originate from three transcriptional units. (ii) H8-5P, H15, H17, H18, H26, and H27 accumulated during reactivation. Of this group, only H26 and H27 could be detected in productively infected cells. (iii) Of the 18 we have examined, only 10 miRNAs were found to accumulate above background levels in productively infected cells. The disparity in the accumulation of miRNAs in cell culture and during reactivation may reflect differences in the patterns of regulation of viral gene expression during productive infection and during reactivation from the latent state.

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