Identification of SARS-CoV-2 Inhibitors using Lung and Colonic Organoids

As SARS-CoV-2 primarily infects the respiratory tract, investigators developed a lung organoid model using human pluripotent stem cells, and generated complementary hPSC-derived colonic organoids to explore the response of colonic cells to SARS-CoV-2 infection.
[Nature]
Han, Y., Duan, X., Yang, L., Nilsson-Payant, B. E., Wang, P., Duan, F., Tang, X., Yaron, T. M., Zhang, T., Uhl, S., Bram, Y., Richardson, C., Zhu, J., Zhao, Z., Redmond, D., Houghton, S., Nguyen, D.-H. T., Xu, D., Wang, X., … Chen, S. (2020). Identification of SARS-CoV-2 Inhibitors using Lung and Colonic Organoids. Nature, 1–8. https://doi.org/10.1038/s41586-020-2901-9 Cite
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The SARS-CoV-2 Targets by the PscRNA Profiling of ACE2, TMPRSS2 and Furin Proteases

Scientists incorporated the protein information to analyze the expression of ACE2, the SARS-CoV-2 receptor, together with co-factors, TMPRSS2 and Furin, at single cell level in situ, which they called protein-proofed single-cell RNA (pscRNA) profiling.
[iScience]
Zhou, L., Niu, Z., Jiang, X., Zhang, Z., Zheng, Y., Wang, Z., Zhu, Y., Gao, L., Huang, H., Wang, X., & Sun, Q. (2020). The SARS-CoV-2 targets by the pscRNA profiling of ACE2, TMPRSS2 and Furin proteases. IScience, 0(0). https://doi.org/10.1016/j.isci.2020.101744 Cite
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Development and Characterization of Rat Duodenal Organoids for ADME and Toxicology Applications

Investigators optimized and characterized rat duodenal organoids with light and electron microscopy, immunofluorescence and notably, global mRNA expression.
[Toxicology]
Hedrich, W. D., Panzica-Kelly, J. M., Chen, S.-J., Strassle, B., Hasson, C., Lecureux, L., Wang, L., Chen, W., Sherry, T., Gan, J., & Davis, M. (2020). Development and characterization of rat duodenal organoids for ADME and toxicology applications. Toxicology, 152614. https://doi.org/10.1016/j.tox.2020.152614 Cite
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Interplay Among p21Waf1/Cip1, MUSASHI-1 and Krüppel-Like Factor 4 in Activation of Bmi1-CreER Reserve Intestinal Stem Cells After Gamma Radiation-Induced Injury

Bmi1-specific Klf4 deletion resulted in decreased numbers of MSI1+ cells in regenerating crypts compared to those of control mice. Researchers showed that KLF4 bound to the Msi1 promoter and activated its expression in vitro.
[Scientific Reports]
Interplay among p21 Waf1/Cip1 , MUSASHI-1 and Krüppel-like factor 4 in activation of Bmi1-Cre ER reserve intestinal stem cells after gamma radiation-induced injury | Scientific Reports. (n.d.). Retrieved October 27, 2020, from https://www.nature.com/articles/s41598-020-75171-w Cite
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Molecular Mechanisms of Calcium‐Mediated Small Intestinal Glucose and Sodium Absorption through the CICR and the SOCE

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]
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
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Extracellular Cyclic Dinucleotides Induce Polarized Responses in Barrier Epithelial Cells by Adenosine Signaling

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]
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
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Exogenous L-Arginine Increases Intestinal Stem Cell Function through CD90+ Stromal Cells Producing mTORC1-Induced Wnt2b

Scientists utilized mice and small intestinal organoid models to clarify the role of L-arginine on epithelial differentiation of intestinal stem cells (ISCs). They showed that L-arginine increased expansion of ISCs in mice.
[Communications Biology]
Hou, Q., Dong, Y., Huang, J., Liao, C., Lei, J., Wang, Y., Lai, Y., Bian, Y., He, Y., Sun, J., Sun, M., Jiang, Q., Wang, B., Yu, Z., Guo, Y., & Zhang, B. (2020). Exogenous L-arginine increases intestinal stem cell function through CD90+ stromal cells producing mTORC1-induced Wnt2b. Communications Biology, 3(1), 1–16. https://doi.org/10.1038/s42003-020-01347-9 Cite
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IL-8/CXCR2 Mediates Tropism of Human Bone Marrow-Derived Mesenchymal Stem Cells toward CD133+/CD44+ Colon Cancer Stem Cells

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]
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
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Roles of Src Family Kinase, Ras, and mTOR Signaling in Intestinal Epithelial Homeostasis and Tumorigenesis

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.
[Cancer Science]
Matozaki, T., Kotani, T., Murata, Y., & Saito, Y. (n.d.). Roles of Src family kinase, Ras, and mTOR signaling in intestinal epithelial homeostasis and tumorigenesis. Cancer Science, n/a(n/a). https://doi.org/10.1111/cas.14702 Cite
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Transcriptional Programmes Underlying Cellular Identity and Microbial Responsiveness in the Intestinal Epithelium

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]
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
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IL-22 Receptor Signaling in Paneth Cells Is Critical for Their Maturation, Microbiota Colonization, Th17-Related Immune Responses, and Anti-Salmonella Immunity

Using novel Paneth cell-specific IL-22Ra1 knockout mice, researchers showed that IL-22 signaling in Paneth cells was required for small intestinal host defense. They showed that Paneth cell maturation, antimicrobial effector function, expression of specific WNTs, and organoid morphogenesis were dependent on cell-intrinsic IL-22Ra1 signaling.
[Mucosal Immunology]
Gaudino, S. J., Beaupre, M., Lin, X., Joshi, P., Rathi, S., McLaughlin, P. A., Kempen, C., Mehta, N., Eskiocak, O., Yueh, B., Blumberg, R. S., van der Velden, A. W. M., Shroyer, K. R., Bialkowska, A. B., Beyaz, S., & Kumar, P. (2020). IL-22 receptor signaling in Paneth cells is critical for their maturation, microbiota colonization, Th17-related immune responses, and anti- Salmonella immunity. Mucosal Immunology, 1–13. https://doi.org/10.1038/s41385-020-00348-5 Cite
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