Scientists found that deletion of Erk1/2 in intestinal epithelial cells at embryonic stages resulted in an unexpected increase in cell proliferation and migration, expansion of intestinal stem cells and formation of polyp-like structures, leading to postnatal death.
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ERK/MAPK signaling is essential for intestinal development through Wnt pathway modulation | Development. (n.d.). Retrieved August 7, 2020, from https://dev.biologists.org/content/early/2020/07/30/dev.185678 Cite
In the wound healing assay, berberine exhibited the ability to promote cell migration, indicating that berberine could probably recover the function of intestinal epithelial cells when the intestinal epithelial barrier was damaged by the peritoneal dialysis fluid.
[Journal of Ethnopharmacology]
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Zhang, D., Jiang, L., Wang, M., Jin, M., Zhang, X., Liu, D., Wang, Z., Yang, L., & Xu, X. (2020). Berberine inhibits intestinal epithelial barrier dysfunction in colon caused by peritoneal dialysis fluid by improving cell migration. Journal of Ethnopharmacology, 113206. https://doi.org/10.1016/j.jep.2020.113206 Cite
Intestinal exposure to inositol trisphosphate and phytate ingestion both promoted recovery following intestinal damage. Remarkably, inositol trisphosphate also induced growth of patient-derived intestinal organoids, stimulated HDAC3-dependent proliferation, and countered butyrate inhibition of colonic growth.
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This review discusses the underlying molecular and cellular underpinnings that control programmed cell death in intestinal epithelial cells, which emerge during intestinal diseases.
[Nature Reviews Gastroenterology & Hepatology]
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Scientists studied the pathways that regulate activating transcription factor 6 and its role for inflammation in intestinal epithelial cells.
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Investigators explored the effects of alginate oligosaccharides on the integrity and migration of small intestine cells using swine intestinal epithelial IPEC-J2 cells.
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In addition to its known microbicidal action, cathelicidin had a unique pathogen-sensing role, facilitating LPS-mediated intestinal responses, including the production of CXCL8/CXCL1 that would contribute to an integrated tissue response to recruit neutrophils during colitis.
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In mice with dextran sodium sulfate or T cell-induced colitis, loss of histocompatibility complex class II (MHCII) from Intestinal epithelial cells reduced but does not eliminated mucosal inflammation. However, in mice with C rodentium-induced colitis, loss of MHCII reduced bacterial clearance by decreasing binding of IgA to commensal and pathogenic bacteria.
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Scientists report a nonpyroptotic role of full-length Gasdermin D in guiding the release of IL-1β–containing small extracellular vesicles from intestinal epithelial cells .
[Journal of Clinical Investigation]
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Scientists revealed CD47 as a negative regulator in intestinal epithelial cell renewal during colitis through downregulating OSKM transcriptional factors.
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Investigators showed that upon Adherent-invasive E. coli (AIEC) infection, intestinal epithelial cells(IECs) secreted exosomes that could transfer specific miRNAs to recipient IECs, inhibiting autophagy-mediated clearance of intracellular AIEC.
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Investigators revealed that Wnt activity triggered the expression of the gene, LARGE2, which in turn mediated the laminin- adhesive O-glycosylation of α-DG. They found abnormally increased cellular adhesion to laminin during Wnt-driven cancer progression.
[Cell Communication and Signaling]
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