Using the intestine of SAMP1/YitFcsJ mice aged 10 to 14 weeks, morphometric alterations in the crypt-villus architecture, intestinal stem cells, crypt cells, and differentiated cells; organoid formation capacity of intestinal crypts; and niche signaling pathways were analyzed and compared with those of age-matched control AKR/J mice.
[Inflammatory Bowel Diseases]
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Lee, C., Hong, S. N., Kim, E. R., Chang, D. K., & Kim, Y.-H. (n.d.). Depletion of Intestinal Stem Cell Niche Factors Contributes to the Alteration of Epithelial Differentiation in SAMP1/YitFcsJ Mice With Crohn Disease-Like Ileitis. Inflammatory Bowel Diseases. https://doi.org/10.1093/ibd/izaa314 Cite
Scientists summarize recent advances in understanding the correlation between Hippo–YAP signaling and intestinal homeostasis, repair, and tumorigenesis, focusing specifically on intestinal stem cell regulation.
The authors describe a new proximity-based profiling method that relies upon a GAL4 driver, termed intestinal-kickout (I-KCKT)-GAL4 , exclusively expressed in intestinal progenitor cells.
Bacainn Therapeutics, Inc. announced the successful completion of the company’s Phase I, first-in-human clinical trial of BT051, a novel, orally administered, gut-selective inhibitor of migration and activation of neutrophils.
[Bacainn Therapeutics, Inc. (Business Wire, Inc.)]
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Deciphera Pharmaceuticals, Inc. announced the completion of its target enrollment in the INTRIGUE Phase III clinical study evaluating the efficacy and safety of QINLOCK in patients with second-line gastrointestinal stromal tumor.
[Deciphera Pharmaceuticals, Inc.]
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Researchers used Mucin-2 (Muc2) knockout mice predisposed to colitis to study intestinal barrier upon chronic inflammation. They used 4-kDa FITC-Dextran assay and transmission electron microscopy to demonstrate the increased intestinal permeability and morphological defects in intercellular junctions in Muc2 knockout mice.
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Borisova, M. A., Achasova, K. M., Morozova, K. N., Andreyeva, E. N., Litvinova, E. A., Ogienko, A. A., Morozova, M. V., Berkaeva, M. B., Kiseleva, E., & Kozhevnikova, E. N. (2020). Mucin-2 knockout is a model of intercellular junction defects, mitochondrial damage and ATP depletion in the intestinal epithelium. Scientific Reports, 10(1), 21135. https://doi.org/10.1038/s41598-020-78141-4 Cite
Scientists aimed to assess the expression of the most common intestinal CYP enzymes in a human induced pluripotent stem cell-derived human intestinal organoid model, and the suitability of that model to study chemical-induced changes in CYP expression and activity.
[Archives of Toxicology]
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Janssen, A. W. F., Duivenvoorde, L. P. M., Rijkers, D., Nijssen, R., Peijnenburg, A. A. C. M., van der Zande, M., & Louisse, J. (2020). Cytochrome P450 expression, induction and activity in human induced pluripotent stem cell-derived intestinal organoids and comparison with primary human intestinal epithelial cells and Caco-2 cells. Archives of Toxicology. https://doi.org/10.1007/s00204-020-02953-6 Cite
Scientists examined the mechanisms of action of LGR4 and LGR5 in parallel using coimmunoprecipitation, proximity ligation, competition binding, and time-resolved FRET assays in whole cells.
Ginsenoside Rb1 (GRb1) administration not only normalized Hrd1 expression at both the mRNA and protein levels, but also alleviated the endoplasmic reticulum stress response, Fas-related apoptosis, and other colitis symptoms. In intestinal cell line IEC-6, the expression of Hrd1 was significantly decreased by LPS treatment, but was normalized by GRb1.
[Acta Pharmacologica Sinica]
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Dong, J., Xia, K., Liang, W., Liu, L., Yang, F., Fang, X., Xiong, Y., Wang, L., Zhou, Z., Li, C., Zhang, W., Wang, J., & Chen, D. (2020). Ginsenoside Rb1 alleviates colitis in mice via activation of endoplasmic reticulum-resident E3 ubiquitin ligase Hrd1 signaling pathway. Acta Pharmacologica Sinica, 1–11. https://doi.org/10.1038/s41401-020-00561-9 Cite
Investigators provide evidence that a thermogenic fat–epithelial cell axis regulates intestinal disease tolerance during experimental colitis. They found that intestinal disease tolerance is a metabolically expensive trait, whose expression was restricted to thermoneutral mice and was not transferable by the microbiota.
[Proceedings of the National Academy of Sciences of the United States of America]
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Man, K., Bowman, C., Braverman, K. N., Escalante, V., Tian, Y., Bisanz, J. E., Ganeshan, K., Wang, B., Patterson, A., Bayrer, J. R., Turnbaugh, P. J., & Chawla, A. (2020). A thermogenic fat-epithelium cell axis regulates intestinal disease tolerance. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.2012003117 Cite
Responses to the inhibitor of apoptosis protein antagonist Birinapant and oxaliplatin/5-fluorouracil were investigated in 14 colon cancer cell lines, representing the consensus molecular subtypes.
[Cell Death & Disease]
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Fichtner, M., Bozkurt, E., Salvucci, M., McCann, C., McAllister, K. A., Halang, L., Düssmann, H., Kinsella, S., Crawford, N., Sessler, T., Longley, D. B., & Prehn, J. H. M. (2020). Molecular subtype-specific responses of colon cancer cells to the SMAC mimetic Birinapant. Cell Death & Disease, 11(11), 1–16. https://doi.org/10.1038/s41419-020-03232-z Cite