Transcriptome analysis of hiHepPCs in various culture conditions, human liver-derived hepatocytes, human liver-derived cholangiocytes, HUVECs, and HPBECs
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PROVIDER: PRJNA494323 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptome analysis of human induced hepatic progenitor cells (hiHepPCs) in various culture conditions, human liver-derived hepatocytes, human liver-derived cholangiocytes, human umbilical vein endothelial cells (HUVECs), and human peripheral blood-derived endothelial cells (HPBECs) We found that a specific combination of three transcription factors, FOXA3, HNF1A, and HNF6, could convert HUVECs and HPBECs into cells that closely resembled hepatic progenitor cells in vitro. These hiHepPCs were expandable in long-term culture and able to differentiate into hepatocytes and cholangiocytes in accordance with their culture conditions. We conducted RNA-seq analyses to investigate the characteristincs of hiHepPCs and their progenies, in addition to those of parental HUVECs, HPBECs, and human liver-derived cells.
2020-08-12 | GSE120732 | GEO
Project description:We report on the successful generation of functional ciliated cholangoocytes from hPSCs that will provide new opportunities to study and treat diseases of the liver. Both monolayer- and organoid-derived cells are adaptable for further bioengineering approcahes to produce more complex hPSC-deived liver tissue with biliary ductal structures. Additionally, the successful engraftment of differentiated cholangiocytes in the liver of immune-imcompetent mice provides the basis for developing novel therapeutic strategies to treat cholangiopathies.
2021-10-03 | GSE175502 | GEO
Project description:Background & Aims: polycystic liver diseases (PLDs) are genetic disorders characterized by progressive development of multiple fluid-filled biliary cysts. Most PLD-causative genes participate in protein biogenesis and/or transport. Post-translational modifications (PTMs) are implicated in protein stability, localization and activity, contributing to human pathobiology; however, their role in PLD is unknown. Here, we aimed to unveil the role of protein SUMOylation in PLD and its potential therapeutic targeting. Methods: levels and function of SUMOylation, along with response to S-adenosylmethionine (SAMe, inhibitor of the SUMOylation enzyme UBC9) and/or short-hairpin RNAs (shRNAs) against UBE2I (UBC9), were evaluated in vitro, in vivo and/or in patients with PLD. SUMOylated proteins were determined by immunoprecipitation and proteomic analyses by mass spectrometry. Results: most SUMOylation-related genes were found overexpressed (mRNA) in polycystic human and rat liver tissue, as well as in cystic cholangiocytes in culture compared to controls. Increased SUMOylated protein levels were also observed in cystic human cholangiocytes in culture, which decreased after SAMe administration. Chronic treatment of polycystic (PCK: Pkdh1-mut) rats with SAMe halted hepatic cystogenesis and fibrosis, and reduced liver/body weight ratio and liver volume. In vitro, both SAMe and shRNA-mediated UBE2I knockdown increased apoptosis and reduced cell proliferation of cystic cholangiocytes. High-throughput proteomic analysis of SUMO1-immunoprecipitated proteins in cystic cholangiocytes identified candidates involved in protein biogenesis, ciliogenesis and proteasome degradation. Accordingly, SAMe hampered the proteasome hyperactivity in cystic cholangiocytes, leading to the activation the unfolded protein response (UPR) and stress-related apoptosis.
2020-09-29 | PXD021140 | Pride
Project description:Background & Aims: polycystic liver diseases (PLDs) are genetic disorders characterized by progressive development of multiple fluid-filled biliary cysts. Most PLD-causative genes participate in protein biogenesis and/or transport. Post-translational modifications (PTMs) are implicated in protein stability, localization and activity, contributing to human pathobiology; however, their role in PLD is unknown. Here, we aimed to unveil the role of protein SUMOylation in PLD and its potential therapeutic targeting. Methods: levels and function of SUMOylation, along with response to S-adenosylmethionine (SAMe, inhibitor of the SUMOylation enzyme UBC9) and/or short-hairpin RNAs (shRNAs) against UBE2I (UBC9), were evaluated in vitro, in vivo and/or in patients with PLD. SUMOylated proteins were determined by immunoprecipitation and proteomic analyses by mass spectrometry. Results: most SUMOylation-related genes were found overexpressed (mRNA) in polycystic human and rat liver tissue, as well as in cystic cholangiocytes in culture compared to controls. Increased SUMOylated protein levels were also observed in cystic human cholangiocytes in culture, which decreased after SAMe administration. Chronic treatment of polycystic (PCK: Pkdh1-mut) rats with SAMe halted hepatic cystogenesis and fibrosis, and reduced liver/body weight ratio and liver volume. In vitro, both SAMe and shRNA-mediated UBE2I knockdown increased apoptosis and reduced cell proliferation of cystic cholangiocytes. High-throughput proteomic analysis of SUMO1-immunoprecipitated proteins in cystic cholangiocytes identified candidates involved in protein biogenesis, ciliogenesis and proteasome degradation. Accordingly, SAMe hampered the proteasome hyperactivity in cystic cholangiocytes, leading to the activation the unfolded protein response (UPR) and stress-related apoptosis.
2020-09-29 | PXD021139 | Pride
Project description:Differentially expressed miRNAs between hepatocytes (GFP-neg in SOX9-GFP mice) and cholangiocytes (GFP-pos in SOX9-GFP mice) in mice at E18.5. We want to compare miRNA population in biliary cells and parenchymal cells (depleted from hematopoietic cells) during liver development. Cholangiocytes specifically express the transcription factor Sox9. This enables to separate cholangiocytes from the rest of the liver parenchyma by FACS from Sox9-GFP transgenic mice. In conclusion, we want to compare miRNA population in our GFP+ cells (cholangiocytes) and our GFP- cells (liver parenchyma depleted from hematopoietic cells).
2018-12-20 | GSE100145 | GEO
Project description:Purpose: The aim of this study is to propose a computational model which can help in unravelling the mechanisms of initial bile duct lumen formation. Guided by the quantification of morphological features and expression of genes in developing bile ducts (cholangiocytes) from embryonic mouse liver, hypotheses for the mechanisms of biliary lumen formation were generated and tested with the model. Here, the RNA-sequencing data were collected from purified embryonic cholangiocytes at two developmental stages (E16 and E18).
2021-05-31 | GSE163062 | GEO
Project description:Gene expression profile analysis allowed to identify a panel of genes and pathways characteristic of hESC-and HepaRG-derived cholangiocytes.
2013-10-28 | GSE51791 | GEO
Project description:Alcoholic hepatitis (AH) is a life-threatening disease with limited treatment options. The presence of cholestasis worsens prognosis but the responsible mechanism is unknown. AH results in infiltration of polymorphonuclear neutrophils (PMNs) in the liver, and cholestasis often reflects bile duct pathology, so we investigated whether and how PMNs interact with cholangiocytes in AH.
2020-03-13 | GSE146899 | GEO
Project description:To study the cancer exosome-induced changes in HUVECs, we characterized the transcriptomes in HUVECs treated with exosomes derived from hypoxia-induced MDA-MB-231. We found the exosomes upregulated the epithelial–mesenchymal transition(EMT)-related and metabolism-related genes in HUVECs.
2021-05-19 | GSE153694 | GEO
Project description:scRNA-seq of primary human adult liver, primary human fetal liver (5 post conceptional weeks), EPCAM+ MACS sorted primary human intrahepatic duct cholangiocytes, sequential timepoints of hiPSC-derived hepatocyte-like cells (HLC), sequential timepoints of hiPSC-derived cholangiocyte-like cells (CLC), sequential timepoints of hiPSC-derived hepatic stellate-like cells (HSLC), sequential timepoints of hiPSC-derived endothelial-like cells (ELC), sequential timepoints of hiPSC-derived macrophage-like cells (MLC) and lentiviral transduced hiPSC-derived hepatocyte-like cells.
2022-05-04 | E-MTAB-8210 | biostudies-arrayexpress