Summary
Endothelial cell-cell junctions play an important role in vascular hemostasis. The
two junctional proteins VE-cadherin and JAM-1 are localized at adherens and tight
junctions, respectively. VE-cadherin is only expressed by endothelial cells, suggesting
that it can exert cell specific function. Absence of VE-cadherin or blocking of its
adhesive activity prevents a normal organization of new vascular structures, suggesting
that VE-cadherin may be a molecular target of antiangiogenic therapy. In addition,
the ability of permeability-increasing agents and adherent leukocytes to modify VE-cadherin/catenin
organization may be related to a role in the control of vascular permeability and
leukocyte infiltration. JAM-1 is an integral membrane protein expressed in endothelial
and epithelial cells. Its extracellular domain can dimerize and bind homophilically.
The intracellular domain (and in particular a PDZ-binding motif) enables JAM-1 to
interact with structural and signaling proteins. Study of the molecular interactions
of JAM-1 may help explain mechanisms of JAM-mediated function, such as control of
paracellular permeability and leukocyte transmigration.
Key words
Endothelium - angiogenesis - permeability - inflammation - adherens and tight junctions