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J. Biol. Chem., Vol. 276, Issue 19, 16223-16231, May 11, 2001
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From the Division of Cardiovascular Medicine, Stanford University
School of Medicine, Stanford, California, 94305 and
§ The First Department of Internal Medicine, Kobe University
School of Medicine, Kobe 650-0017, Japan
To gain fundamental information regarding the
molecular basis of endothelial cell adhesive interactions during
vascular formation, we have cloned and characterized a unique cell
adhesion molecule. This molecule, named endothelial cell-selective
adhesion molecule (ESAM), is a new member of the immunoglobulin
superfamily. The conceptual protein encoded by cDNA clones consists
of V-type and C2-type immunoglobulin domains as well as a hydrophobic
signal sequence, a single transmembrane region, and a cytoplasmic
domain. Northern blot analysis showed ESAM to be
selectively expressed in cultured human and murine vascular endothelial
cells and revealed high level expression in lung and heart and low
level expression in kidney and skin. In situ hybridization
analysis indicated that ESAM is primarily expressed in the
developing vasculature of the embryo in an endothelial cell-restricted
pattern. Epitope-tagged ESAM was shown to co-localize with cadherins
and catenins in cell-cell junctions. In aggregation assays employing
ESAM-expressing Chinese hamster ovary cells, this novel molecule was
shown to mediate cell-cell adhesion through homophilic interactions.
The endothelial cell-selective expression of this immunoglobulin-like
adhesion molecule coupled with its in vitro functional
profile strongly suggests a role in cell-cell interactions that is
critical for vascular development or function.
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) human ESAM, AF361746 and mouse ESAM, AF361882.
Cloning of an Immunoglobulin Family Adhesion Molecule Selectively
Expressed by Endothelial Cells*
§,,
*
This work was supported by a grant from the American Heart
Association.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
These authors contributed equally to this work and should be
considered co-first authors.
¶
To whom correspondence should be addressed: Division of
Cardiovascular Medicine, Falk CVRC, Stanford University Medical School, 300 Pasteur Dr., Stanford, CA 94305. Tel.: 650-723-5013; Fax: 650-725-2178; E-mail: tomq1@leland.stanford.edu.
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