Role of Integrins in Enterocyte Migration

Abstract

1. Enterocyte motility depends critically on cell-matrix interactions. Although still incompletely understood, these appear critically dependent upon integrin-mediated cell adhesion. 2. In addition to providing a mechanism for cell adhesion and traction, the integrins are likely to serve as true receptors for the matrix across which cell motility occurs, initiating signals by both mechanical and chemical means that alter cell phenotype and proliferation as well as cell motility. 3. Sound rationale now exists to postulate that soluble growth factors within the extracellular milieu regulate intestinal mucosal healing not only directly but also indirectly by modulating integrin expression and organization.

Interactions of Escherichia coli strains of non-EPEC serogroups that carry eae and lack the EAF and stx gene sequences with undifferentiated and differentiated intestinal human Caco-2 cells

“…In vivo, several physiological and pathological factors are known to disrupt the epithelial barrier [19]. When the injury is con¢ned to the mucosa, the ¢rst response is the rapid induction of epithelial migration, a process termed restitution [20]. Cells involved in this process decrease or rearrange the expression of many di¡erentiation characteristics, especially basolateral molecules involved in the cell^cell and cell^matrix interactions.…”

Paradigms for Mechanical Signal Transduction in the Intestinal Epithelium

“…However, small mucosal wounds also occur constantly during normal gut function, perhaps because of friction with mucosal contents [18]. Such mucosal injuries result in restitution, a process by which intestinal epithelial cells adjacent to the mucosal wound flatten out, become squamous in morphology, extend lamellipodia, and migrate across the defect in order to resurface it [41, 42]. Such substantial morphologic changes are also likely to cause physical deformation of these intestinal epithelial cells.…”

Rotavirus Replication in Intestinal Cells Differentially Regulates Integrin Expression by a Phosphatidylinositol 3-Kinase-Dependent Pathway, Resulting in Increased Cell Adhesion and Virus Yield

“…Differentiated epithelial cells on villi in the small intestine (enterocytes) are the main targets of infection, leading to cell death, a reduction in villus epithelium area, loss of absorptive capacity, and osmotic dysregulation (3,7,48,53). Enterocytes are attached to the basement membrane through interactions between the basement matrix and cell-surface adhesion molecules, mainly members of the integrin family (4,6,49,64). Increased enterocyte loss is a feature of rotavirus disease, suggesting that reduced enterocyte adhesion occurs (9).…”