Researchers uncovered a novel role of T cell–stem/transient amplifying cell contact in intestinal stem cell (ISC) fate decisions. They showed that intestinal lymphocyte depletion results in skewed ISC differentiation in mice, which can be rescued by T cell transfer.
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Researchers showed that a high-fat diet reduced the expression of the major histocompatibility complex class II genes in intestinal epithelial cells, including intestinal stem cells.
[Cell Stem Cell]
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The authors generated Strap intestinal epithelial knockout mice by crossing mice containing floxed alleles of Strap with Villin-Cre mice. They used human colon cancer cell lines and human and mouse colon tumor-derived organoids for STRAP knockdown/knockout and overexpression experiments.
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Mouse intestinal organoids and dextran sulfate sodium-induced colitis mouse model were used to assess the effects of recombinant soluble thrombomodulin on proliferation of intestinal epithelial cells.
[Clinical Gastroenterology and Hepatology]
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Based on the results of a bibliometric analysis of intestinal organoids applications, scientists systematically summarized the latest advances and analyzed the limitations and prospects.
[Frontiers in Cell and Developmental Biology]
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Scientists demonstrated that inhibition of a high fat diet (HFD)-activated fatty acid oxidation program created a therapeutic opportunity to counter the effects of a HFD on intestinal stem cells and intestinal tumorigenesis.
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Apc-mutant intestinal stem cell (ISCs) functioned as bona fide supercompetitors by secreting WNT antagonists, thereby inducing differentiation of neighbouring wild-type ISCs.
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The authors review recent findings on how adult intestinal stem cells differentiate, interact with their environment, and change during aging.
[Current Opinion in Cell Biology]
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Researchers showed that restricted chromatin accessibility in intestinal stem cells prevented the expression of β-Catenin-regulated metabolic enzymes, whereas fine-tuning of WNT/β-Catenin activity by ZNRF3 and RNF43 restricted proliferation in chromatin-permissive AXIN2+ hepatocytes, while preserving metabolic function.
[Cell Stem Cell]
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Researchers employed a doxycycline-inducible phosphatase of regenerating liver-3 (PRL-3) mouse strain to show that aberrant PRL-3 expression within a non-cancerous background led to the death of Lgr5+ intestinal stem cells and to Paneth cell expansion.
[Journal of Molecular Medicine]
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By targeting antiapoptotic proteins with specific BH3 mimetics in organoid models of colorectal cancer progression, scientists found that BCL-2 was essential only during instestinal stem cell transformation while MCL1 inhibition did not affect adenoma outgrowth.
[Cell Death & Differentiation]
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