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(American Journal of Pathology. 2000;157:1955-1962.)
© 2000 American Society for Investigative Pathology

Regular Articles

Ligation of {alpha}4ß1 Integrin on Human Intestinal Mucosal Mesenchymal Cells Selectively Up-Regulates Membrane Type-1 Matrix Metalloproteinase and Confers a Migratory Phenotype

Sylvia L. F. Pender*, Mikko T. Salmela{dagger}, Giovanni Monteleone*, Denni Schnapp*, Catriona McKenzie*, Jo Spencer{ddagger}, Sherman Fong§, Ulpu Saarialho-Kere{dagger} and Thomas T. MacDonald*

From the Centre for Infection, Allergy, Inflammation and Repair,*
University of Southampton School of Medicine, Southampton, United Kingdom; the Department of Dermatology,{dagger}
Helsinki University Central Hospital, Helsinki, Finland; the Department of Histopathology,{ddagger}
King’s, Guy’s and St. Thomas’ School of Medicine, London, United Kingdom; and Genentech Incorporated,§
South San Francisco, California

Human intestinal lamina propria mesenchymal cells show high surface expression of the {alpha}4ß1 integrin. Ligation of {alpha}4ß1 on mesenchymal cell lines with an activating monoclonal anti-{alpha}4 antibody or vascular cell adhesion molecule-immunoglobulin (VCAM-IgG) leads to the appearance of activated forms of gelatinase A in culture supernatants, and the de novo expression of activated membrane type-1-matrix metalloproteinase (MT1-MMP). In functional assays, signaling through {alpha}4ß1 results in an increased capacity of mesenchymal cells to migrate through an artificial extracellular matrix, an effect inhibitable by excess tissue inhibitor of metalloproteinase-2. In organ cultures of human intestine, VCAM-IgG also up-regulates MT1-MMP, and in mucosal ulcers of inflammatory bowel disease patients, MT1-MMP transcripts are abundant, coincident with expression of VCAM-1 on cells at the ulcer margin. Collectively these results suggest that {alpha}4ß1-induced up-regulation of MT1-MMP may be a crucial factor in the migration of mesenchymal cells into ulcer beds during restitution of diseased gut mucosa.




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