Epithelial Cell Migration in the Intestine

Abstract

Despite significant advances in our understanding of the roles of the cytoskeleton and matrix receptors in cell locomotion, derived largely from in vitro studies on the movement of epithelial cell sheets and isolated cells, the mechanism of epithelial cell migration in the adult intestine remains an enigma. The primary function of the epithelial cell cytoskeleton seems to be in the maintenance of the apical region of the epithelium facing the gut lumen. There we find the brush border, with its associated enzymes, and the intercellular adhesion complexes that give the epithelium its cohesiveness and its barrier function. Curiously, there is little in the way of an organized cytoskeleton in the basal region of the epithelium adjacent to the basement membrane on which the epithelium is presumed to migrate. In this short review, I focus on what is known about epithelial migration from our understanding of the structure of the epithelium and from studies on wound healing, and indicate some avenues for future study.

Intestinal gene expression profiles of piglets benefit from maternal supplementation with a yeast mannan-rich fraction during gestation and lactation

“…The enrichment of these functions is in agreement with previous studies that have shown intestinal development gene expression profiles during early life affected by maternal nutrition during gestation (Meyer et al, 2013). Our results also reported different functions related to inhibition in cell migration; these functions should be interpreted as regular development as opposed to the process of migration that in most cases is associated with an injury or inflammation response (Heath, 1996). Survival of connective tissue was reported to be in an activation state and may represent positive structural development of the intestinal tract (Ishizuya-Oka and Shimozawa, 1992).…”

Depolarization and decreased surface expression of K+ channels contribute to NSAID-inhibition of intestinal restitution

“…Early mucosal restitution, as manifest by the rapid resealing of superficial wounds secondary to cell migration is an important primary repair modality, critical to preserving GI mucosal integrity [17][18][19][20]. NSAIDs contribute to ulcer formation and delay ulcer healing by inhibiting intestinal epithelial cell migration and mucosal restitution [14][15][16].…”

“…Superficial mucosal defects typically are repaired rapidly by migration of epithelial cells into the defect from the periphery of the wound. This process, called mucosal restitution, is a primary repair modality in the GI tract and is critical to preserving mucosal integrity and to suppressing ulceration [17][18][19][20]. Restitution occurs within minutes to hours following injury in vivo or in vitro, because this process requires cell migration but not cell proliferation or differentiation [17][18][19][20].…”

“…This process, called mucosal restitution, is a primary repair modality in the GI tract and is critical to preserving mucosal integrity and to suppressing ulceration [17][18][19][20]. Restitution occurs within minutes to hours following injury in vivo or in vitro, because this process requires cell migration but not cell proliferation or differentiation [17][18][19][20]. While it is established that NSAIDs promote ulceration by interfering with restitution [14][15][16], the signaling pathways mediating this effect have not been fully elucidated.…”

Genus-Specific Substitution Rate Variability among Picornaviruses

“…85, 2011 NOTES 7945 nal tissue, which has the highest turnover rate of all adult mammalian tissues (24,65). This speculation is also supported by the fact that the fastest-evolving nonenterovirus, HPeV, frequently infects enteric tissue (15,56) and was once classified as an enterovirus (15,56).…”