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10.1038/s41598-017-02190-5

http://scihub22266oqcxt.onion/10.1038/s41598-017-02190-5
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C5446415!5446415!28550311
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suck abstract from ncbi


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pmid28550311      Sci+Rep 2017 ; 7 (ä): ä
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  • Organoid-based epithelial to mesenchymal transition (OEMT) model: from an intestinal fibrosis perspective #MMPMID28550311
  • Hahn S; Nam MO; Noh JH; Lee DH; Han HW; Kim DH; Hahm KB; Hong SP; Yoo JH; Yoo J
  • Sci Rep 2017[]; 7 (ä): ä PMID28550311show ga
  • The current in vitro or in vivo intestinal fibrosis models have many limitations. Recent advancements in the isolation and culturing of organoids has led to development of various three-dimensional (3D) intestinal disease models with in vivo physiology. In this study, we generated an organoid-based epithelial to mesenchymal transition (OEMT) model, which could be used as a novel intestinal fibrosis model. Intestinal epithelial organoids (IEOs) were isolated and cultured from the small intestines of normal mice. IEOs were treated with transforming growth factor- ?1 (TGF-?1) or Tumor necrosis factor-? (TNF-?) to evaluate their phenotypic change. Raw 264.7 cells (macrophage) stimulated with lipopolysaccharide were co-cultured with IEOs in growth media with or without TGF-?1. TGF-?1 alone slightly induced epithelial to mesenchymal transition (EMT) in the IEOs but mainly disrupted them. Macrophage released cytokines synergistically induced mesenchymal phenotypic changes in TGF-?1 stimulated intestinal organoids. TNF-? and TGF-?1 synergistically induced proliferation of mesenchymal cells as well as EMT in the IEOs. We generated a novel OEMT model based on our finding that TNF-? and TGF-? synergistically induce type 2 EMT in IEOs. This 3D EMT model with in vivo physiology could be used to study EMT associated intestinal fibrosis.
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