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Dystroglycan is involved in laminin‐1‐stimulated motility of Müller glial cells: Combined velocity and directionality analysis
Author(s) -
Méhes Elöd,
Czirók András,
Hegedüs Balázs,
Szabó Bálint,
Vicsek Tamás,
Satz Jakob,
Campbell Kevin,
Jancsik Veronika
Publication year - 2005
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20135
Subject(s) - dystroglycan , laminin , biology , microbiology and biotechnology , motility , integrin , glycoprotein , extracellular matrix , neuroscience , cell , biochemistry
We investigate the role of dystroglycan, a major laminin‐1 receptor and central member of the dystrophin–glycoprotein complex, in the laminin‐1 induced motility of cultured Müller glial cells. Binding of laminin‐1 to dystroglycan was prevented by IIH6, a function‐blocking monoclonal antibody against α‐dystroglycan. As an alternative means of inhibition, we used heparin to mask the dystroglycan binding site of the laminin‐1, known to overlap with heparin binding sites. Cell motility was characterized in a two‐dimensional motility assay based on computer‐controlled videomicroscopy and statistical analysis of cellular trajectories. We obtained data on both the cell velocity and the diffusion index, a measure of direction‐changing frequency. Both means of inhibition of dystroglycan function led to a significant decrease in the ability of laminin‐1 to stimulate cell migration. At the same time, dystroglycan function does not appear to be involved in laminin‐1‐dependent increase in process dynamism and direction‐changing activity. © 2004 Wiley‐Liss, Inc.