Exact(1)
Together, these studies add validation to the presence of an endogenous mechanism used by the intestinal epithelium to dynamically regulate its paracellular permeability properties and better define the potential to enhance the oral delivery of biopharmaceuticals via a transient regulation of an endogenous mechanism controlling the intestinal paracellular barrier.
Similar(59)
This new approach combining microengineered scaffolds, biophysical cues and chemical gradients to control the intestinal epithelium ex vivo can serve as a physiologically relevant mimic of the human small intestinal epithelium, and is broadly applicable to model other tissues that rely on gradients for physiological function.
Therefore, treatment is aimed at controlling the permanent intestinal inflammation.
These scenarios are not mutually exclusive, and it is possible that the EGFR pathway separately modulates the integration of new enterocytes into the epithelia and their elimination by sloughing, thereby controlling the flux of intestinal cells.
Nevertheless, the role of TLR signaling in controlling the composition of the intestinal microbiota remains controversial.
Ascl2 is a Wnt-responsive master transcription factor that controls the Lgr5 intestinal stem cell gene expression program.
The intestinal mucosal epithelium acts as a cellular barrier between the gut and the intestinal lumen, controlling the passage of ions, molecules and microorganisms.
Our data suggest that IL-22RA1 plays a role in controlling the systemic dissemination of intestinal bacteria, particularly a potential opportunistic E. faecalis species, during infectious and noninfectious intestinal injuries.
Intestinal bacteria and their metabolites, including short-chain fatty acids (SCFAs), butyric acid in particular, exert significant physiological effects on the host by controlling the differentiation and proliferation of intestinal epithelial cells, providing energy to epithelial cells, modulating the immune system, and protecting against pathogens [6] [10].
Recently, we identified the receptor tyrosine kinase MET as a target of Wnt signalling, suggesting a role for MET in controlling the turnover and differentiation of intestinal epithelium (Boon et al, 2002).
Despite numerous findings on the role of Wnt signaling in controlling the maintenance and plasticity of intestinal stem and progenitor cells (ISPCs), mechanistic studies on the influence of Wnt/β-catenin signaling on the maintenance of ISPC in the context of DNA damage have not been reported.
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