Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1230784 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Hepatocytes have wide applications in drug development, disease modeling, and cell therapy. However, to expand hepatocytes in large quantities in vitro without losing their functions remains a challenging task. Here we report that IL22, a cytokine highly upregulated after partial hepatectomy or hepatocyte transplantation, could support long-term expansion (>30 passages, with theoretical expansion of ~1030 times within ~150 days) of mice hepatocytes in vitro by dedifferentiate hepatocytes into hepatocyte progenitor cells (HPCs), which maintain the capacity of differentiation into mature hepatocytes. With transcriptomic analysis and lineage-specific deletion, we uncover the critical involvement of STAT3 pathway in IL22-mediated hepatocyte to HPC conversion. Two key transcription factors (TFs) down-stream of STAT3 pathway, Bhlha15 and Arntl2, govern IL22-induced hepatic dedifferentiation. Expression of these two TFs directly initiates the dedifferentiation of hepatocytes into HPCs, which could be expanded in long-term without the supplement of IL22. IL22 also supports human hepatocyte growth in simple culture condition. Within 30 days, human hepatocytes could be expanded by more than 10,000-fold by dedifferentiation into HPCs, which maintain the full capacity of maturation. Collectively, this study provides a simple culture system enables large-scale expansion of both mice and human hepatocytes in vitro, and elucidates the critical pathways and TFs involved in these processes.
2025-03-06 | GSE290952 | GEO
Project description:To investigate the influence of hepatocellular STAT3 activation on liver under alcohol condiction, mice of Stat3 condictional knock-out in hepatocytes were treated by alcohol for 2 weeks.
2023-07-28 | GSE224602 | GEO
Project description:IL22 induces genome-wide Stat3 binding in primary mouse hepatocytes in vitro [ChIP-Seq] (Mus musculus)
| PRJNA1369386 | ENA
Project description:Purpose: Here we report the differential gene expression profile between WT and C3G knock out E14Tg2a cells. The cells were grown in equel seeding density in GMEM Serum +LIF media. RNA was isolated after 48 hr and sequenced Methods: C3G knock out E14Tg2a mouse ES cells were made by CrisprCAS9 mediated knock out strategy. RNA was collected using Trizol method from WT and knock out clone 48 hr after seeding in equel density in a 6 well plate, precoated with gelatin. Results: Using an optimized data analysis workflow, we mapped about 75 million sequence reads per sample to the mouse genome (build mm10) and identified 5797 genes were differentially expressed with adjusted p-value < 0.05(significant) between the WT and C3G-/-. Approximately 17% of the genes showed differential expression between the WT and C3g−/− ESCs, with a fold change ≥1.5 and p value <0.05. Biological pathways and gene ontology enrichment analysis of differentially expressed genes reveals that C3G is required to maintain adhesion of ES cells and for differentiation of mouse ES cells. Conclusions: The study revealed the first transcriptome profile of C3G gene knock out in E14Tg2a mouse embryoinic tem cells. In our study we found that C3G acts as a mediaator of differentiation by activatingERK and integrin signaling and supressing STAT3 and other pluripotency factors like ESRRB and KLF4.
2021-06-21 | GSE159595 | GEO
Project description:Mouse liver tumors (T) and non tumoral adjacent livers (NT) sorted from mice knock out for Axin1 gene specifically in the hepatocytes . 3 mice of the brother hood non deleted for Axin1 were used as controls (WT) We used microarrays to determine the differential expression between tumoral and non tumoral tissue.
2018-03-13 | GSE107374 | GEO
Project description:Differentiation of human organoids with IL22, and/or the inhibition of the same process with STAT3 or mTOR inhibitors.
2022-10-13 | PXD028746 | Pride
Project description:Mitochondria control bioenergetics and cell fate decisions, but whether they also participate in extra-organelle signaling is not understood. Here, we show that interference with cyclophilin D (CypD), a mitochondrial matrix protein and apoptosis regulator, causes accelerated cell proliferation and enhanced cell migration and invasion. These responses are associated with global transcriptional changes in CypD-/- cells, predominantly affecting chemokines and their receptors, and resulting in increased activating phosphorylation of Signal Transduction and Activator of Transcription 3 (STAT3). In turn, STAT3 signaling promotes increased proliferation of CypD-/- cells via accelerated S-phase entry and supports Cxcl12-directed paracrine cell motility. Therefore, mitochondria-to-nuclei transcriptional signaling globally affects cell division and motility. As immunosuppressive therapies often target CypD, this pathway may predispose the tissue microenvironment of these patients to oncogenic transformation. Three wild type (WT) and three CypD-/- knock-out mouse embryonic fibroblasts (MEFs) have been compared.
2013-03-08 | E-GEOD-41280 | biostudies-arrayexpress