Abstract
Several stem cell markers within the gastrointestinal epithelium have been identified in mice. One of the best characterized is Lgr5 (leucine-rich repeat-containing G-protein coupled receptor 5) and evidence suggests that Lgr5+ cells in the gut are the origin of gastrointestinal cancers. Reserve or facultative stem or progenitor cells with the ability to convert to Lgr5+ cells following injury have also been identified. Unlike the intestine, where Lgr5+ cells at the crypt base act as active stem cells, the stomach may contain unique stem cell populations, since gastric Lgr5+ cells seem to behave as a reserve rather than active stem cells, both in the corpus and in the antral glands. Gastrointestinal stem cells are supported by a specific microenvironment, the stem cell niche, which also promotes tumorigenesis. This review focuses on stem cell markers in the gut and their supporting niche factors. It also discusses the molecular mechanisms that regulate stem cell function and tumorigenesis.
Highlights
One of the best characterized is Lgr5 and evidence suggests that Lgr5+ cells in the gut are the origin of gastrointestinal cancers
Intestinal stem cells (ISCs) in mice were identified in earlier label-retention assays, in which a nucleic acid analog was administered in combination with epithelial damage, such as irradiation [2]
While the administration of R-spondin, a ligand for Lgr5, inhibits the expansion and tracing of Lgr5-derived clones, it promotes lineage tracing by Axin2+ cells. These findings suggest that R-spondin inhibits stem cell function in Lgr5+ cells and/or that it activates Axin2+ cells via other receptors, such as Lgr4
Summary
Self-renewal and pluripotency are cardinal properties of stem cells [1]. In the gastrointestinal system, the integrity of the epithelium is maintained by long-lived stem cells. Intestinal stem cells (ISCs) in mice were identified in earlier label-retention assays, in which a nucleic acid analog was administered in combination with epithelial damage, such as irradiation [2]. After the discovery of intestinal Lgr5+ stem cells, gastric Lgr5-expressing cells were identified in the antral gland base (i.e., below the antral isthmus). These apparently self-renewing, multipotent cells supply their daughter cells upwards from the base [16]. It has been proposed that gastric chief cells which express Lgr and reside at the corpus gland base may act as a reserve stem cell after epithelial injury [17]. R-spondin activates antral isthmal stem cells but inhibits Lgr expressing stem cells
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