Breast cancer derived Evs cause liver fibrosis. [II]
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ABSTRACT:
PROVIDER: PRJNA1094904 | ENA |
REPOSITORIES: ENA
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Project description:breast cancer derived Evs carried NT5C2 to liver tissue, which causes inosine accumulation in liver. High inosine level suppressed ADAR1-P150 protein level and decreased global A-I editing level. Fibronectin-1 displayed a higher mRNA level due to the reduction of splicing sites' editing. Overall, breast cancer derived EVs cause liver fibrosis.
2025-01-01 | GSE262917 | GEO
Project description:Breast cancer derived Evs cause liver fibrosis. [I]
| PRJNA1093377 | ENA
Project description:breast cancer derived Evs carried NT5C2 to liver tissue, which causes inosine accumulation in liver. High inosine level suppressed ADAR1-P150 protein level and decreased global A-I editing level. Fibronectin-1 displayed a higher mRNA level due to the reduction of splicing sites' editing. Overall, breast cancer derived EVs cause liver fibrosis.
2025-01-01 | GSE262782 | GEO
Project description:EVs derived from HPCs could affect the progression of S. japonicum-induced fibrosis. Considering the EVs’ cargo, small RNAs account for a large proportion of cargoes in EVs, and act as one of the critical post-transcriptional regulators in cell-to-cell communication. Among them, miRNAs are the most studied and their regulatory roles in host–pathogen interactions are increasingly clear. HPCs are a kind of stem cells with potentially bidirectional differentiation ability and interact with hepatic stellate cells during liver injury. The activation of HPCs play an important role during S. japonicum-induced liver fibrosis. We used microarrays to detail the gene expression of SEA-EVs and CON-EVs derived from HPC cell line, LE/6.
2024-04-07 | GSE245873 | GEO
Project description:Renal tubular epithelial cells are the main cells affected in the process of renal fibrosis, and it has been shown that mesenchymal stem cell-derived exosomes can treat renal fibrosis, and then the traditional 2D-EVs production method is inefficient. We efficiently extracted 3D-EVs by coaxial bioprinting, but the mechanism of 3D-EVs for treating renal fibrosis is not yet known. Therefore, we used TGF-beta1 to induce a renal fibrosis phenotype in NRK-52E cells and took 2D- and 3D-EVs for treatment in order to explore the possible differential molecular mechanisms of 2D- and 3D-EVs for renal fibrosis. This approach facilitates the discovery of new mechanisms for exosomes to treat renal fibrosis.
2024-12-18 | GSE281863 | GEO
Project description:Aims Biliary diseases represent around 10% of all chronic liver diseases and affect both adults and children. Currently available biochemical tests detect cholestasis but not early liver fibrosis. Circulating extracellular vesicles (EVs) provide a real-time molecular snapshot of the injured organ in a non-invasive way. We thus aimed at searching for a panel of EV-based biomarkers for cholestasis-induced early liver fibrosis using mice models. Results: Progressive and detectable histological evidence of collagen deposition and liver fibrosis was observed as from Day 8 after bile duct ligation (BDL) in mice. Whole transcriptome and small RNA-seq analyses of circulating EVs revealed differentially enriched RNA species after BDL versus sham controls. Unsupervised hierarchical clustering identified a signature that allowed for discrimination between BDL and controls. In particular, 151 microRNAs enriched in BDL-derived EVs were identified, of which 66 were conserved in humans. The liver was an important source of circulating EVs in BDL animals as evidenced by the enrichment of several hepatic mRNAs, such as Albumin, Haptoglobin, Transferrin receptor 1 and Alas2. Interestingly, among experimentally validated miRNAs, miR194-5p and miR29-3p showed similar enrichment patterns also in EVs derived from DDC-treated (drug-induced cholestasis) and MDR2-/- (genetic cholestasis) mice. Innovation A panel of mRNAs and miRNAs contained in circulating EVs, when combined, provides sensitive biomarkers for the early detection of hepatic damage and fibrosis. Conclusion Analysis of EVs for enrichment in miR29-3p and miR194-5p, in combination with hepatic injury RNA markers, could represent a sensitive biomarker panel for the early detection of cholestasis-induced liver fibrosis.
2022-02-28 | GSE166753 | GEO
Project description:Aims Biliary diseases represent around 10% of all chronic liver diseases and affect both adults and children. Currently available biochemical tests detect cholestasis but not early liver fibrosis. Circulating extracellular vesicles (EVs) provide a real-time molecular snapshot of the injured organ in a non-invasive way. We thus aimed at searching for a panel of EV-based biomarkers for cholestasis-induced early liver fibrosis using mice models. Results: Progressive and detectable histological evidence of collagen deposition and liver fibrosis was observed as from Day 8 after bile duct ligation (BDL) in mice. Whole transcriptome and small RNA-seq analyses of circulating EVs revealed differentially enriched RNA species after BDL versus sham controls. Unsupervised hierarchical clustering identified a signature that allowed for discrimination between BDL and controls. In particular, 151 microRNAs enriched in BDL-derived EVs were identified, of which 66 were conserved in humans. The liver was an important source of circulating EVs in BDL animals as evidenced by the enrichment of several hepatic mRNAs, such as Albumin, Haptoglobin, Transferrin receptor 1 and Alas2. Interestingly, among experimentally validated miRNAs, miR194-5p and miR29-3p showed similar enrichment patterns also in EVs derived from DDC-treated (drug-induced cholestasis) and MDR2-/- (genetic cholestasis) mice. Innovation A panel of mRNAs and miRNAs contained in circulating EVs, when combined, provides sensitive biomarkers for the early detection of hepatic damage and fibrosis. Conclusion Analysis of EVs for enrichment in miR29-3p and miR194-5p, in combination with hepatic injury RNA markers, could represent a sensitive biomarker panel for the early detection of cholestasis-induced liver fibrosis.
2022-02-28 | GSE166752 | GEO
Project description:Translational control of cardiac fibrosis (II)
| PRJNA542670 | ENA
Project description:Liver fibrosis is characterized by the activation of perivascular hepatic stellate cells (HSCs), the release of fibrogenic nano-sized extracellular vesicles (EVs) and increased HSC glycolysis. Nevertheless, how glycolysis in HSCs coordinates fibrosis amplification through tissue zone-specific pathways remains elusive. Here, we demonstrate that HSC-specific genetic inhibition of glycolysis reduced liver fibrosis. Moreover, spatial transcriptomics revealed a fibrosis-mediated upregulation of EV-related pathways in the liver pericentral zone, which was abrogated by the glycolysis genetic inhibition. Mechanistically, glycolysis in HSCs upregulated the expression of EV-related genes such as RAB31 by enhancing histone-3-lysine-9 acetylation on the promoter region, which increased EV release. Functionally, these glycolysis-dependent EVs increased fibrotic gene expression in recipient HSC. Furthermore, EVs derived from glycolysis-deficient mice abrogated liver fibrosis amplification in contrast to glycolysis-competent mouse EVs. In summary, glycolysis in HSCs amplifies liver fibrosis by promoting fibrogenic EV release in the hepatic pericentral zone, which represents a potential therapeutic target.
2024-05-16 | PXD050337 | Pride