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Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114
Epithelial cell
kinase (Eck) is a member of a large family of receptor tyrosine kinases
whose functions remain largely unknown. Expression and regulation of
Eck and its cognate ligand B61 were analyzed in the human colonic
adenocarcinoma cell line Caco-2. Immunocytochemical staining
demonstrated coexpression of Eck and B61 in the same cells, suggestive
of an autocrine loop. Eck levels were maximal in preconfluent cells. In
contrast, B61 levels were barely detectable in preconfluent cells and
increased progressively after the cells reached confluence. Caco-2
cells cultured in the presence of added B61 showed a significant
reduction in the levels of dipeptidyl peptidase and sucrase-isomaltase
mRNA, markers of Caco-2 cell differentiation. Cytokines
interleukin-1
(IL-1), basic fibroblast growth factor, IL-2,
epidermal growth factor, and transforming growth factor- modulated
steady-state levels of Eck and B61 mRNA and regulated Eck activation as
assessed by tyrosine phosphorylation. Functionally,
stimulation of Eck by B61 resulted in increased proliferation, enhanced
barrier function, and enhanced restitution of injured epithelial
monolayers. These results suggest that the Eck-B61 interaction, a
target of regulatory peptides, plays a role in intestinal epithelial
cell development, migration, and barrier function, contributing to
homeostasis and preservation of continuity of the epithelial barrier.
growth factors; cytokines; receptors; differentiation
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