Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA192945 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A non-functional myosin Vb motor in duodenal enterocytes results in disruption of epithelial cell polarity characterized by complete loss of microvilli and mislocalization of apical brush border proteins in the cytoplasm which finally cause a devastating disease in neonates with severe malabsorption defects accompanied by protracted diarrhea during infancy, classified as microvillus inclusion disease (MVID). The exact mechanisms how loss-of-function of MYO5B induces polarity loss are not completely understood in MVID pathogenesis. Obtaining better insights in cell polarity defects caused by loss of MYO5B, we performed microarray- in combination with protein expression-analysis in an inducible CaCo2 MYO5B RNAi cell system. Surprisingly, in MYO5B-depleted CaCo2 cells, CDH1 coding for the cell adhesion protein E-Cadherin and important for cell adhesion and therefore maintenance of cell polarity, was significantly downregulated. Interestingly, mesenchymal cell markers, specifically Vimentin and N-Cadherin, physiologically not expressed in differentiated epithelium, were upregulated and accompanied by increased phospho-c-jun levels in the nucleus. Importantly phospho-c-jun was also found in nuclei of duodenal enterocytes in MVID patients, indicating loss of MYO5B induces epithelial cell scattering in enterocytes. 3 Myosin 5B KD versus 3 control samples
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Project description:A non-functional myosin Vb motor in duodenal enterocytes results in disruption of epithelial cell polarity characterized by complete loss of microvilli and mislocalization of apical brush border proteins in the cytoplasm which finally cause a devastating disease in neonates with severe malabsorption defects accompanied by protracted diarrhea during infancy, classified as microvillus inclusion disease (MVID). The exact mechanisms how loss-of-function of MYO5B induces polarity loss are not completely understood in MVID pathogenesis. Obtaining better insights in cell polarity defects caused by loss of MYO5B, we performed microarray- in combination with protein expression-analysis in an inducible CaCo2 MYO5B RNAi cell system. Surprisingly, in MYO5B-depleted CaCo2 cells, CDH1 coding for the cell adhesion protein E-Cadherin and important for cell adhesion and therefore maintenance of cell polarity, was significantly downregulated. Interestingly, mesenchymal cell markers, specifically Vimentin and N-Cadherin, physiologically not expressed in differentiated epithelium, were upregulated and accompanied by increased phospho-c-jun levels in the nucleus. Importantly phospho-c-jun was also found in nuclei of duodenal enterocytes in MVID patients, indicating loss of MYO5B induces epithelial cell scattering in enterocytes.
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Project description:The generation of pancreatic organoids from human pluripotent stem cells represents a major breakthrough for regenerative medicine and the modeling of diseases such as diabetes. However, current approaches remain inefficient due to lengthy multi-step differentiation protocols and limited functional maturity in the organoids. In this study, we overcome these challenges using multi-phase optimization screens to achieve rapid generation of functionally mature pancreatic organoids from a stable endocrine progenitor culture. We conducted stepwise culture condition screens that enabled the stable culture of multiple pancreatic progenitor cell states, including the unprecedented stable propagation of NEUROD1-expressing endocrine progenitor-like cells (EpSCs). Further transcriptomic profiling of EpSC confirmed similarity of that to previously reported endocrine progenitor populations. Using EpSCs, we significantly reduced the number of steps and timing required to generate pancreatic organoids, enabling rapid testing of conditions for organoid maturation. Utilizing this optimized protocol, we further tested conditions to promote pancreatic organoid maturation. We identified that exosome-delivered WNT5B, in combination with RSPO1 (exoW/R), could strongly induce non-canonical WNT/JNK signaling, promoting pancreatic organoid maturation. This combinatorial exosome treatment enhances epithelial organization, reduces immature cell states, and significantly improves glucose responsiveness and insulin secretion. Collectively, our work establishes a robust pancreatic differentiation platform that integrates long-term progenitor expansion with optimized organoid maturation. This system provides a reproducible experimental framework for studying pancreatic development, investigating disease mechanisms, and facilitating future translational applications involving pancreatic organoids.
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Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
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Project description:We have sequenced miRNA libraries from human embryonic, neural and foetal mesenchymal stem cells. We report that the majority of miRNA genes encode mature isomers that vary in size by one or more bases at the 3’ and/or 5’ end of the miRNA. Northern blotting for individual miRNAs showed that the proportions of isomiRs expressed by a single miRNA gene often differ between cell and tissue types. IsomiRs were readily co-immunoprecipitated with Argonaute proteins in vivo and were active in luciferase assays, indicating that they are functional. Bioinformatics analysis predicts substantial differences in targeting between miRNAs with minor 5’ differences and in support of this we report that a 5’ isomiR-9-1 gained the ability to inhibit the expression of DNMT3B and NCAM2 but lost the ability to inhibit CDH1 in vitro. This result was confirmed by the use of isomiR-specific sponges. Our analysis of the miRGator database indicates that a small percentage of human miRNA genes express isomiRs as the dominant transcript in certain cell types and analysis of miRBase shows that 5’ isomiRs have replaced canonical miRNAs many times during evolution. This strongly indicates that isomiRs are of functional importance and have contributed to the evolution of miRNA genes
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