Cell Migration and Polarity on Microfabricated Gradients of Extracellular Matrix Proteins

Langmuir ◽  
2006 ◽  
Vol 22 (9) ◽  
pp. 4250-4258 ◽  
Author(s):  
Rico C. Gunawan ◽  
Jonathan Silvestre ◽  
H. Rex Gaskins ◽  
Paul J. A. Kenis ◽  
Deborah E. Leckband
1997 ◽  
Vol 23 (2) ◽  
pp. 102-112 ◽  
Author(s):  
R. Mahesparan ◽  
B. B. Tysnes ◽  
K. Edvardsen ◽  
H. K. Haugeland ◽  
I. Garcia Cabrera ◽  
...  

Pancreas ◽  
2009 ◽  
Vol 38 (7) ◽  
pp. 804-810 ◽  
Author(s):  
Eduard Ryschich ◽  
Akmal Khamidjanov ◽  
Vachtang Kerkadze ◽  
Markus W. Büchler ◽  
Margot Zöller ◽  
...  

1993 ◽  
Vol 14 (4) ◽  
pp. 158-161 ◽  
Author(s):  
Wilson Savino ◽  
Dea Maria S. Villa-Verde ◽  
Joseli Lannes-Vieira

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2215-2215
Author(s):  
Valentin P. Yakubenko ◽  
Tatiana P. Ugarova

Abstract Integrin αDβ2 (CD11d/CD18), the most recently discovered member of the β2 sub-family of adhesion receptors, is strongly upregulated on macrophage foam cells which underscores its potential role in atherosclerosis. However, the contribution of αDβ2 to monocyte/macrophage adhesive reactions and the significance of its overexpression on these cells remain unknown. Recently we characterized αDβ2 as a multiligand receptor capable of binding many extracellular matrix proteins with the recognition specificity overlapping that of the major myeloid-specific integrin αMβ2 (Mac-1). We hypothesized that the αDβ2 ability to bind numerous ligands in the extracellular matrix and its capacity to be upregulated to high density on the surface of macrophages may modulate cell adhesiveness and, thus, affect migration. To evaluate the role of αDβ2 in migration, we generated model and natural cells expressing different densities of αDβ2 and tested their migration to different extracellular matrix proteins. In vitro studies demonstrated that αDβ2 expressed at low densities, either on the surface of HEK293 cells or the mouse macrophage cell line IC-21, supported migration which was partially inhibited by anti-αD function-blocking antibodies. Furthermore, β1 and β3 integrins expressed on HEK293 cells and IC-21 macrophages, respectively, contributed to migration because anti-β1 and anti-β3 antibodies inhibited migration. Increased expression of αDβ2 on the surface of HEK293 cells and its upregulation by PMA on IC-21 macrophages resulted in the inhibition of cell migration. Ligation of αDβ2 with anti-αD antibodies restored β1- and β3-driven cell migration by means of removing restraints imposed by the excess of the αDβ2-ligand adhesive bonds. To test the possibility that progressive upregulation of αDβ2 can block macrophage migration in vivo, we assessed the effect of anti-αD function blocking antibodies using the thioglycollate-induced peritonitis model. More than 4-fold upregulation of αDβ2 was detected on macrophages in 72 h after thioglycollate stimulation and, similar to in vitro studies, the numbers of migration macrophages increased in the presence of anti-αD antibodies. These results demonstrate that the density of αDβ2 can modulate cell migration and suggest that low levels of αDβ2 can contribute to monocyte migration while αDβ2 upregulation on differentiated macrophages might facilitate their retention at the site of inflammation.


1997 ◽  
Vol 23 (3) ◽  
pp. 102-112 ◽  
Author(s):  
R. Mahesparan ◽  
B. B. Tysnes ◽  
K. Edvardsen ◽  
H. K. Haugeland ◽  
I. Garcia Cabrera ◽  
...  

2021 ◽  
Vol 22 (17) ◽  
pp. 9177
Author(s):  
Jing Yang Tee ◽  
Alan Mackay-Sim

Cell migration is critical for brain development and linked to several neurodevelopmental disorders, including schizophrenia. We have shown previously that cell migration is dysregulated in olfactory neural stem cells from people with schizophrenia. Although they moved faster than control cells on plastic substrates, patient cells were insensitive to regulation by extracellular matrix proteins, which increase the speeds of control cells. As well as speed, cell migration is also described by directional persistence, the straightness of movement. The aim of this study was to determine whether directional persistence is dysregulated in schizophrenia patient cells and whether it is modified on extracellular matrix proteins. Directional persistence in patient-derived and control-derived olfactory cells was quantified from automated live-cell imaging of migrating cells. On plastic substrates, patient cells were more persistent than control cells, with straighter trajectories and smaller turn angles. On most extracellular matrix proteins, persistence increased in patient and control cells in a concentration-dependent manner, but patient cells remained more persistent. Patient cells therefore have a subtle but complex phenotype in migration speed and persistence on most extracellular matrix protein substrates compared to control cells. If present in the developing brain, this could lead to altered brain development in schizophrenia.


2004 ◽  
Vol 216 (03) ◽  
Author(s):  
U Schüller ◽  
W Hartmann ◽  
A Koch ◽  
K Schilling ◽  
OD Wiestler ◽  
...  

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