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Junctional adhesion molecule‐A regulates cell migration and resistance to shear stress
Author(s) -
Huang Hayden,
Cruz Francisco,
Bazzoni Gianfranco
Publication year - 2006
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.20712
Subject(s) - microbiology and biotechnology , motility , cell adhesion , cell , cell migration , integrin , adhesion , chemistry , biology , biochemistry , organic chemistry
Junctional adhesion molecule‐A (JAM‐A) is an adhesive protein expressed in endothelial cells, epithelial cells, platelets, and some leukocytes. JAM‐A localizes to the tight junctions between contacting endothelial and epithelial cells, where it contributes to cell–cell adhesion and to the control of paracellular permeability. JAM‐A also regulates cell motility, even though the quantitative biophysical features have not been characterized. In this study, we evaluated the role of JAM‐A in the regulation of cell motility using JAM‐A‐expressing and JAM‐A‐deficient murine endothelial cells. We report that, in the absence of shear stress, JAM‐A absence increases cell motility by increasing directional persistence but not cell speed. In addition, in the presence of shear stress, JAM‐A absence increases protrusion extension in the direction of flow and increased downstream cellular displacement (while, conversely, decreasing upstream displacement). All these effects of JAM‐A absence are mitigated by the microtubule‐stabilizing compound taxol. A motility‐ and microtubule‐related function, integrin‐mediated adhesiveness, was only slightly reduced in JAM‐A‐deficient cells compared with JAM‐A‐expressing cells. However, overexpression of JAM‐A in the JAM‐A‐deficient cells increased integrin adhesiveness to the same levels as those observed in taxol‐treated JAM‐A‐deficient cells. Taken together, these data indicate that JAM‐A regulates cell motility by cooperating with microtubule‐stabilizing pathways. J. Cell. Physiol. 209: 122–130, 2006. © 2006 Wiley‐Liss, Inc.