Ontology highlight
ABSTRACT:
PROVIDER: PRJNA288336 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2078810.fastq.gz | Fastqsanger.gz | |||
| SRR2078820.fastq.gz | Fastqsanger.gz | |||
| SRR2078801.fastq.gz | Fastqsanger.gz | |||
| SRR2078811.fastq.gz | Fastqsanger.gz | |||
| SRR2078821.fastq.gz | Fastqsanger.gz |
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Project description:Partial Hepatectomy Induced Long Noncoding RNA Inhibits Hepatocyte Proliferation during Liver Regeneration
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Project description:1. Evaluate the diagnostic value of long noncoding RNA (CCAT1) expression by RT-PCR in peripheral blood in colorectal cancer patients versus normal healthy control personal.
2. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in diagnosis of colorectal cancer patients & its relation to tumor staging.
3. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in precancerous colorectal diseases.
4. Compare long noncoding RNA (CCAT1) expression with traditional marker; carcinoembryonic antigen (CEA) and Carbohydrate antigen 19-9 (CA19-9) in diagnosis of colorectal cancer.
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Project description:Liver regeneration following resection is a complex process relying on coordinated pathways and cell types in the remnant organ. Myeloid-Derived Suppressor Cells (MDSCs) have a role in liver regeneration-related angiogenesis but their influence on hepatocyte proliferation and immune modulation during liver regeneration is unclear. We examined the transcriptional response of regenerating liver hepatocytes after major resection in mice with CD11b+Ly6G+ MDSCs (G-MDSCs) depletion using RNA sequencing. Global gene expression profiling of regenerating hepatocytes upon G-MDSC depletion revealed disrupted transcriptional progression from day one to day two after major liver resection. Key genes and pathways related to hepatocyte proliferation and immune response were differentially expressed upon MDSC depletion. This study provides evidence that MDSCs contribute to early liver regeneration by promoting hepatocyte proliferation and modulating the intra-liver immune response. These findings illuminate the multifaceted role of MDSCs in liver regeneration.
2024-09-29 | GSE277186 | GEO
Project description:Dynamic remodeling of translation programs drives hepatocyte proliferation during liver regeneration
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Project description:Long non-coding RNAs (lncRNAs) play important roles in the regulation of many biological processes in the cell like transcription, translation, splicing, transport, etc. More than 10K lncRNAs are predicted in human, but functions for the majority remain unknown. LncRNAs may contribute to the development of multiple diseases that makes them perspective diagnostic and prognostic markers as well as drug targets [1]. Murine lncRNA Falcor/LL35 is a proposed functional analog of human lncRNA DEANR1, which is predominantly expressed in murine lungs and liver, intestine and pancreas [2, 3]. While the participation of LL35 in LL35–Foxa2 (transcription factor) regulatory loop during regeneration after lung injury was previously described by Swarr et al. [2], its functional role in murine liver remains unknown. In our work we focused on revealing the role of murine lncRNA LL35 in hepatocytes and in mouse liver. We analyzed changes in proteome of AML12 (normal hepatocytes) cell line on the 2nd day after LL35 depletion. [1] Morlando, M., Ballarino, M., & Fatica, A. (2015). Long non-coding RNAs: New players in hematopoiesis and leukemia. Frontiers in Medicine, Vol. 2. [2] Swarr, D. T., Herriges, M., Li, S., Morley, M., Fernandes, S., Sridharan, A., … Morrisey, E. E. (2019). The long noncoding RNA Falcor regulates Foxa2 expression to maintain lung epithelial homeostasis and promote regeneration. Genes & Development, 33(11-12), 656–668. [3] Sergeeva, O. V, Korinfskaya, S. A., Kurochkin, I. I., & Zatsepin, T. S. (2019). Long Noncoding RNA LL35 / Falcor Regulates Expression of Transcription Factor Foxa2 in Hepatocytes in Normal and Fibrotic Mouse Liver. Acta Naturae, 11(42), 66–74.
2022-08-11 | PXD033910 | Pride
Project description:Liver regeneration is an extraordinarily complex process involving a variety of factors; however, the role of chromatin protein in hepatocyte proliferation is largely unknown. In this study, we investigated the functional role of high-mobility group box 2 (HMGB2), a chromatin protein in liver regeneration using wild-type and HMGB2-knockout (KO) mice. Liver tissues were sampled after 70% partial hepatectomy (PHx), and analyzed by immunohistochemistry using various markers of cell proliferation, including Ki-67, PCNA, cyclin D1, cyclin B1, EdU and pH3S10. In WT mice, hepatocyte proliferation was strongly correlated with the spatiotemporal expression of HMGB2; however, cell proliferation was significantly delayed in hepatocytes of HMGB2-KO mice. Quantitative PCR demonstrated that cyclin D1 and cyclin B1 mRNAs were significantly decreased in HMGB2-KO mice livers. Interestingly, hepatocyte size was significantly larger in HMGB2-KO mice at 36-72 h after PHx, and these results suggest that hepatocyte hypertrophy appeared in parallel with delayed cell proliferation. In vitro experiments demonstrated that cell proliferation was significantly decreased in HMGB2-KO cells. A significant delay in cell proliferation was also found in HMGB2-siRNA transfected cells. In summary, spatiotemporal expression of HMGB2 is important for regulation of hepatocyte proliferation and cell size during liver regeneration.
2022-04-03 | GSE199944 | GEO
Project description:The liver has a remarkable capacity for regeneration after injury. Midlobular hepatocytes have been proposed as the most plastic hepatic cell type, providing definitive evidence that zone 2 of the liver lobule acts as a reservoir for hepatocyte proliferation during homeostasis and regeneration. However, the implication of other mechanisms beyond hyperplasia that contribute to liver repair have been little explored and the collaboration of another hepatocyte subpopulation has differed among previous studies depending on the model of liver injury used. Thus, re-examination of dynamics of hepatocytes during regeneration is critical to get a better understanding of underlaying mechanisms for potential cell therapy and treatment of liver diseases. Here, using a mouse model of hepatocyte- and non-hepatocyte-specific multicolor lineage tracing, we demonstrate that hepatocytes located in the midlobular region also undergo hypertrophy besides cell division in response to chemical, physical, and viral insults. Our study shows for first time that this subpopulation also combats liver impairment after infection with coronavirus. Furthermore, we demonstrate that pericentral hepatocyte subpopulation also expands in number and size during the repair process in collaboration with midlobular hepatocytes and Galectin-9-CD44 pathway may be critical for driving these processes. Interestingly, we identified transdifferentiation and cell fusion processes during liver regeneration after severe injury that may be key to recover hepatic function.
2024-01-12 | GSE250568 | GEO
Project description:After 70% partial hepatectomy (PHx), the metabolic pathways leading to hepatocyte lipid droplet accumulation during liver regeneration remain unclear. Aquaporin 5 (Aqp5) is an aquaporin and peroporin that facilitates the transport of both water and hydrogen peroxide (H2O2). In this study, we observed a delayed liver regeneration following PHx in Aqp5 knockout (Aqp5−/−) mice. Considering the role of Aqp5 in H2O2 transport, we hypothesized that deficiency in Aqp5 may induce oxidative stress and hepatocyte injury. Through the measurement of reactive oxygen species (ROS) and redox-related indices, we observed significant alterations in ROS levels as well as malondialdehyde (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH) concentrations in regenerating livers lacking Aqp5 compared to wild-type controls. Oil Red O and 4-hydroxynonenal (4-HNE) staining results indicated that Aqp5 deficiency caused lipid accumulation during liver regeneration. The transcriptome sequencing results showed that the PPAR pathway is inhibited during the liver regeneration process in Aqp5 gene-knockout mice.The administration of the WY-14643 agonist, which targets the PPAR pathway, significantly mitigated delayed liver regeneration by enhancing hepatocyte proliferation and reducing lipid accumulation caused by Aqp5 deficiency. Our findings highlight the crucial role of Aqp5 in regulating H2O2 levels and lipid metabolism through the PPAR pathway during liver regeneration.
2024-12-23 | GSE284995 | GEO
Project description:Spatiotemporal expression of HMGB2 regulates cell proliferation and hepatocyte size during liver regeneration
| PRJNA822301 | ENA
Project description:Transcriptome analysis of mouse whole liver. Array raw data was processed by Transcriptome Analysis Console (TAC) Software. Subsequent analyses, including Gene Ontology analysis and Functional Enrichment Analysis (FEA), were performed using the TAC software and the DAVID platform, leveraging WikiPathways. Gene Set Enrichment Analysis (GSEA) was conducted using GSAE software version 4.3.2. All the results, including the list of Differential Expression Genes (DEGs) and outcomes from the aforementioned analyses, have been documented in Supplementary Data 1 and 2 as Excel files. Given the widespread use of partial hepatectomy for treating various liver pathologies, understanding the mechanisms of liver regeneration is vital for enhancing liver resection and transplantation therapies. Here, we demonstrate the critical role of the serine protease Hepsin in promoting hepatocyte hypertrophy and proliferation. Under steady-state conditions, liver-specific overexpression of Hepsin in adult wild-type mice triggers hepatocyte hypertrophy and subsequent proliferation, significantly increasing liver size. This effect is predominantly driven by the catalytic activity of Hepsin, engaging the EGFR-Raf-MEK-ERK signaling pathway. Significantly, administering Hepsin substantially enhances hepatocyte proliferation and facilitates liver regeneration following a 70% partial hepatectomy. Crucially, the proliferation induced by Hepsin is a transient event, without leading to long-term adverse effects such as liver fibrosis or hepatocellular carcinoma, as evidenced by extensive observation. These results offer substantial potential for future clinical applications and translational research endeavors in the field of liver regeneration post-hepatectomy.
2024-11-30 | GSE245233 | GEO