Glucose absorption and channel expression were examined in mouse upper jejunal epithelium by Ussing chamber study and immunocytochemistry, respectively. Ca2+ and Na+ imaging was also performed in single intestinal epithelial cells.
[British Journal of Pharmacology]
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Molecular Mechanisms of Calcium‐mediated Small Intestinal Glucose and Sodium Absorption through the CICR and the SOCE - Zhang - - British Journal of Pharmacology - Wiley Online Library. (n.d.). Retrieved October 23, 2020, from https://bpspubs.onlinelibrary.wiley.com/doi/10.1111/bph.15287 Cite
Scientists found that cyclic dinucleotides(CDNs) containing adenosine induced a robust CFTR-mediated chloride secretory response together with cAMP-mediated inhibition of Poly I:C-stimulated IFNβ expression. Signal transduction was strictly polarized to the serosal side of the epithelium, dependent on the extracellular and sequential hydrolysis of CDNs to adenosine by the ectonucleosidases ENPP1 and CD73, and occurred via activation of A2B adenosine receptors.
[Proceedings of the National Academy of Sciences of the United States of America]
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Chang, D., Whiteley, A. T., Gwilt, K. B., Lencer, W. I., Mekalanos, J. J., & Thiagarajah, J. R. (2020). Extracellular cyclic dinucleotides induce polarized responses in barrier epithelial cells by adenosine signaling. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.2015919117 Cite
Scientists compared the effects of three tissue‐derived mesenchynal stem cells (MSCs) in vivo on colon tumor xenograft growth. Then, they analyzed the tropism of bone marrow‐derived MSCs toward normal intestinal epithelial cells, parental colon cancer cells, CD133−/CD44−, and CD133+/CD44+ colon cancer cells in vitro.
[Journal of Cellular Physiology]
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Ma, X., Chen, J., Liu, J., Xu, B., Liang, X., Yang, X., Feng, Y., Liang, X., & Liu, J. (n.d.). IL-8/CXCR2 mediates tropism of human bone marrow-derived mesenchymal stem cells toward CD133+/CD44+ Colon cancer stem cells. Journal of Cellular Physiology, n/a(n/a). https://doi.org/10.1002/jcp.30080 Cite
Dysregulation of intestinal epithelial cells(IEC) homeostasis likely contributes to the development of intestinal inflammation and intestinal cancer. The roles of receptor protein tyrosine kinases and their downstream signaling molecules such as Src family kinases, Ras, and mammalian target of rapamycin in homeostatic regulation of IEC turnover have recently been evaluated.
The authors review insights from mice and other vertebrate models into the transcriptional regulatory mechanisms underlying intestinal epithelial identity and microbial responsiveness, including DNA methylation, chromatin accessibility, histone modifications and transcription factors.
[Nature Reviews Gastroenterology & Hepatology]
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Heppert, J. K., Davison, J. M., Kelly, C., Mercado, G. P., Lickwar, C. R., & Rawls, J. F. (2020). Transcriptional programmes underlying cellular identity and microbial responsiveness in the intestinal epithelium. Nature Reviews Gastroenterology & Hepatology, 1–17. https://doi.org/10.1038/s41575-020-00357-6 Cite
The authors verified the applicability of 3D organoids for in vitro investigation of intestinal biochemical processes related to transport and metabolism of nutrients and drugs.
[Frontiers in Bioengineering and Biotechnology]
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Zietek, T., Giesbertz, P., Ewers, M., Reichart, F., Weinmüller, M., Urbauer, E., Haller, D., Demir, I. E., Ceyhan, G. O., Kessler, H., & Rath, E. (2020). Organoids to Study Intestinal Nutrient Transport, Drug Uptake and Metabolism – Update to the Human Model and Expansion of Applications. Frontiers in Bioengineering and Biotechnology, 8. https://doi.org/10.3389/fbioe.2020.577656 Cite
Using pharmacological and genetic perturbations in cultured intestinal epithelial cells, investigators found that non-muscle myosin-2C controls the length of growing microvilli by regulating actin turnover in a manner that requires a fully active motor domain.
[Molecular Biology of the Cell]
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Bile acid‐activated farnesoid X receptor enhanced glucose uptake in intestinal epithelial cells by increasing the expression of glucose transporter 2, which depended on ERK1/2 phosphorylation via S1PR2. However, it also reduced the cell energy generation via inhibition of oxidative phosphorylation, which was crucial for intestinal glucose transport.
[Journal of Cellular and Molecular Medicine]
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Gly‐Pro‐Ala (GPA) alleviates intestinal inflammation and oxidative stress by inhibiting NF‐κB activation. GPA binds to the ligand‐binding domain of Nur77 and stimulates its autotranscriptional activity to enhance its expression in intestinal epithelial cells. Furthermore, GPA activates the promoter of IκBα to increase its expression, resulting in the abolishment of the NF‐κB pathway.
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GPA peptide enhances Nur77 expression in intestinal epithelial cells to exert a protective effect against DSS‐induced colitis - Deng - - The FASEB Journal - Wiley Online Library. (n.d.). Retrieved September 29, 2020, from https://faseb.onlinelibrary.wiley.com/doi/10.1096/fj.202000391RR Cite
Recent studies investigating the role of MHC class II+ exosomes released by Intestinal epithelial cells report conflicting findings of either immune enhancing or immunosuppressive activities. In addition to modulating inflammatory responses, recent findings suggest that MHC class II expression by intestinal stem cells may elicit crosstalk that promotes epithelial renewal.
Hemin catalyzed the formation of reactive oxygen species (ROS) and induced oxidative DNA damage as well as DNA strand breaks in both HCEC and CRC cells. In contrast, inorganic iron hardly affected ROS levels and only slightly increased DNA damage. Hemin, but not inorganic iron, caused cell death and reduced cell viability.
[Cell Death & Disease]
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Seiwert, N., Wecklein, S., Demuth, P., Hasselwander, S., Kemper, T. A., Schwerdtle, T., Brunner, T., & Fahrer, J. (2020). Heme oxygenase 1 protects human colonocytes against ROS formation, oxidative DNA damage and cytotoxicity induced by heme iron, but not inorganic iron. Cell Death & Disease, 11(9), 1–16. https://doi.org/10.1038/s41419-020-02950-8 Cite