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The Role of JAM‐A in Inflammatory Bowel Disease: Unrevealing the Ties That Bind
Author(s) -
Vetrano Stefania,
Danese Silvio
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.04045.x
Subject(s) - tight junction , paracellular transport , microbiology and biotechnology , barrier function , claudin , chemistry , cell junction , pathogenesis , inflammatory bowel disease , homeostasis , extracellular , inflammation , function (biology) , permeability (electromagnetism) , immunology , biology , disease , membrane , medicine , pathology , biochemistry , cell
Tight junctions (TJ) are junctional proteins whose function is to maintain an intact intestinal epithelial barrier and regulate the paracellular movement of water and solutes. Altered TJ structure and epithelial permeability are observed in inflammatory bowel disease and seem to have an important role in the pathogenesis of these diseases. Junctional adhesion molecule‐A (JAM‐A) is a protein expressed at tight junctions of epithelial and endothelial cells, as well as on circulating leukocytes. Its function at tight junctions appears to be crucial as an extracellular adhesive molecule in the direct regulation of intestinal barrier function. This review focuses on the role of JAM‐A in controlling mucosal homeostasis by regulating the integrity and permeability of epithelial barrier function.