Ontology highlight
ABSTRACT:
PROVIDER: PRJNA705692 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13816067.fastq.gz | Fastqsanger.gz | |||
| SRR13816068.fastq.gz | Fastqsanger.gz | |||
| SRR13816069.fastq.gz | Fastqsanger.gz | |||
| SRR13816070.fastq.gz | Fastqsanger.gz | |||
| SRR13816071.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 29 |
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Project description:Selective HIF stabilisation in 70% liver resection
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Project description:ATAC-seq was performed to investigate changes in chromatin accessibility in repsonse to HIF stabilisation via VH298
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Project description:In this work, the effect of splenectomy on liver regeneration was studied. For this purpose in the animals were reproduced splenectomy, and after 7 days 70% liver resection was performed. Animals in which the spleen was intact and only 70% liver resection was performed served as a comparison group. Animals in which only the spleen was removed also served as controls. The animals were removed from the experiment after 24 hours, 3 and 7 days. Macrophages were isolated from the livers of control animals as well as from the liver after 70% resection by magnetic sorting using the F4/80 marker. RNA was isolated from the obtained macrophages and used for transcriptome analysis. Macrophages in the regenerating liver were transcriptomically enriched for signaling pathways associated with monocyte migration, cell adhesion and cell death.
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Project description:In this work, the effect of splenectomy on liver sinusoidal cells was studied. For this purpose in the animals were reproduced splenectomy, and after 7 days 70% liver resection was performed. Animals in which the spleen was intact and only 70% liver resection was performed served as a comparison group. Animals in which only the spleen was removed also served as controls. The animals were removed from the experiment after 24 hours, 3 and 7 days. Liver sinusoidal cells were isolated from the livers of control animals as well as from the liver after 70% resection by magnetic sorting using the CD146 beads. RNA was isolated from the obtained liver sinusoidal cells and used for transcriptome analysis. Liver sinusoidal cells in the regenerating liver were transcriptomically enriched for signaling pathways associated with monocyte migration, cell adhesion and cell death.
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Project description:The aim of our work was to study the expression profile of spleen genes during liver regeneration, to identify possible biologically active substances that affect reparative processes and inflammation in other organs, as well as the state of the monocytic-macrophage and lymphocytic population of the spleen after liver resection. We used microarrays for comparison of spleen gene expression on different time periods after 70% liver resection
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Project description:The liver has the unique capacity to regenerate after surgical resection. However, the regulation of liver regeneration is not completely understood. We performed miRNA microarray analyses of liver tissue from Wistar rats at different time points after 70% partial hepatectomy (0, 2, 6, 12, 24, 48 hours, and 5 days) and after sham laparotomy (12, 24, and 48 hours). We demonstrate that miRNA expression patterns changed during liver regeneration and that these changes were most evident during the peak of DNA replication at 24 hours after resection. Expression of 13 miRNAs, including five members of the let-7 family, was significantly reduced 12-48 hours after resection, whereas 3 miRNAs were significantly upregulated (> 25% change). We provide a temporal miRNA expression dataset of the regenerating rat liver, which indicates a primary function for miRNA during the peak of DNA replication. These data will assist further functional studies on the role of miRNAs during liver regeneration.
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Project description:Study of kidney state in 70% liver resection in experiment in mice
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Project description:The von–Hippel Lindau (VHL) protein is a tumour suppressor protein frequently mutated in the VHL disease, which functions as substrate recognition subunit of a Cul2 E3 ubiquitin ligase (CRL2VHL). CRL2VHL plays an important role in oxygen sensing, by binding and targeting Hypoxia Inducible Factor-alpha subunits (HIF-alpha) for ubiquitination and degradation. VHL is also commonly hijacked by heterobifunctional degrader molecules known as proteolysis-targeting chimeras (PROTACs). In previous work we reported the structure-based design and functional characterisation of VHL inhibitors (VH032 and VH298) that induce the HIF response in cells. Here, we use unbiased quantitative mass spectrometry to identify the proteomic changes elicited by the VHL inhibitor and compare this to hypoxia or broad-spectrum prolyl-hydroxylase domain (PHD) enzyme inhibitor IOX2. Our results demonstrate the VHL inhibitor selectively activates the HIF response that vastly overlaps with hypoxia- and IOX2-induced proteomic changes. Interestingly, VHL inhibitors were found to selectively upregulate a single protein, which is VHL itself. Our analysis revealed that this occurs via protein stabilisation of VHL isoforms and not via changes in transcript levels. Increased VHL levels upon VH298 treatment resulted in turn to reduced levels of HIF-1α protein. Our results demonstrate the high specificity of VHL inhibitors and suggest that use of these inhibitors would not produce overtly side effects due to prolonged HIF stabilisation. They also exemplify the concept that small-molecule binding induced protein stabilisation can increase protein levels inside cells.
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Project description:Acute myeloid leukaemia (AML) is a largely incurable haematological disease, for which new efficient therapeutic strategies are urgently needed. While leukaemogenesis occurs under hypoxic conditions of the bone marrow, the therapeutic tractability of the hypoxia inducible factor (HIF) system in AML is elusive. Given that inactivation of HIF-1α and HIF-2α promotes leukaemic transformation, a possible therapeutic strategy for AML treatment is to constitutively stabilise HIF- α proteins. This can be achieved by targeting the HIF-prolyl hydroxylases (PHDs), the catalysis of which promotes HIF-1α and HIF-2α degradation. Here, we demonstrate that genetic inactivation of Phd1 or Phd2 compromises initiation and progression of AML, without impacting normal haematopoiesis, thus implying the immense therapeutic potential of targeting PHDs in AML. To pharmacologically inactivate PHDs, we employed clinical grade PHD inhibitors as well as a new selective PHD inhibitor (IOX5), which stabilises HIF-α through a novel mechanism of action. Pharmacological PHD inhibition compromises AML cells in a HIF-α dependent manner to disable pro-leukaemogenic pathways in AML cells, re-program their metabolism, and induce cell death, at least in part via pro-apoptotic BNIP3. Importantly, concurrent inhibition of anti-apoptotic BCL-2 by clinically used Venetoclax potentiates the anti-leukaemic effect of PHD inhibition. Thus PHD inhibition with consequent HIF-α stabilisation is a promising new non-toxic strategy for AML treatment.
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Project description:Effect of splenectomy on liver regeneration after 70% resection in a mouse model.
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