Mus musculus breed:Balb/c
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA689858 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Exosomal miRNAs regulated by MSCs in acute-on-chronic liver failure mice
| PRJNA689768 | ENA
Project description:development of prognostic biomarkers for HBV-related acute-on-chronic liver failure
2020-03-07 | PXD017928 |
Project description:Compared to whole serum miRNAs, miRNAs in serum small extracellular vesicles (sEVs) are well protected form RNA enzymes, thus provide a consistent source of miRNA for disease biomarker detection. Serum sEVs and their miRNA cargos released by injured liver cells could be promising biomarkers for diagnosis of liver diseases. We were very interested to find out the effects of liver injury on serum extracellular vesicles as well as the small RNA components they transported, if there is any difference between acute and chronic injury. Study in this regard will help us to identify new serum biomarkers for liver injury, and to find out if there are specific markers for acute or chronic liver injury. To identify potential biomarker for liver injury based on serum sEVs miRNAs, we established the carbon tetrachloride (CCL4) induced acute and chronic liver injury mice model, and examined the dynamic changes of small RNA components, especially miRNAs, in serum sEVs.
2021-08-07 | E-MTAB-9462 | biostudies-arrayexpress
Project description:Molecular characterization of chronic liver disease dynamics: from liver fibrosis to acute-on-chronic liver failure
| PRJNA580468 | ENA
Project description:The key exosomal miRNAs in adaptive response to drug-induced liver (DILI) and liver regeneration were investigated and proved. This study aimed to decipher the mechanism of restorative events in the adaptive response to DILI by investigating circulating exosomal miRNAs. Using toosendanin-induced liver injury model, exosomal miR-106b-5p was identified as a robust driver in the adaptive response of TILI.
2020-11-07 | GSE160961 | GEO
Project description:To explore how tumor-derived exosomes activate fibroblasts and foster lung metastasis of liver cancer. MiRNAs encapsulated in exosomes are abundant and play an important role in cell-cell communication. Therefore, we hypothesized that tumor-derived exosomal miRNAs mediate fibroblasts activation. To identify the specific miRNAs involved, we conducted microarrays to generate miRNAs profiles of exosomes derived from the four liver cancer cell lines with different migration and invasion abilities. CSQT-2 and HCC-LM3 cells were high metastatic cancer cells, versus to HepG2 and MHCC-97L cells. We divided them into the following groups: CSQT-2 versus HepG2 (with different origins), HCC-LM3 versus MHCC-97L (with the same origin) and compared the up-regulated miRNAs in both two high-metastatic cancer cells-derived exosomes. Then, these up-regulated miRNAs were subjected to validation to define the most important exosomal miRNAs in regulating fibroblast activation and contributing to lung metastasis of liver cancer.
2017-11-03 | GSE106452 | GEO
Project description:Acute myeloid leukemia (AML) cells release abundant exosomal miR-7977 that transfer into bone marrow (BM) mesenchymal stromal cells (MSCs). We have shown that exosomal miR-7977 was highly released from AML cells and was transferred into BM MSCs. It has been well known that a microRNA has multiple targets. In fact, miRDB predicted 633 targets. Based on these findings, control and miR-7977mimic were transferred into BM MSCs. Subsequently, alteration of transcriptome was analyzed to gain insight into the role of miR-7977 in bone marrow micro environment.
2019-03-18 | GSE108186 | GEO
Project description:Peripheral infusion of human umbilical cord mesenchymal stem cells (hUC-MSCs) can profoundly suppress the activation of c-Mos and remarkably improve hepatic histology, suppress the systemic inflammatory reaction, and promote animal survival in a large non-human primate model of acute liver failure (ALF). The mechanism through which hUC-MSCs inhibits c-Mos activation in vivo remains unclear. We hypothesized that hUC-MSCs can adaptively produce certain inhibitory cytokines in response to the pro-inflammatory microenvironment. To confirm this, we stimulated cultured hUC-MSCs with inflammatory monkey serum (serum isolated at day 1 following toxin challenge). After a 30-min stimulation, the cells were collected for microarray gene expression analysis. A whole human genome oligo microarray analysis was performed to reveal the altered gene expression profiles of the hUC-MSCs
2016-05-12 | E-MTAB-4750 | biostudies-arrayexpress
Project description:Background/Aim: We investigated alterations in the expression of serum exosomal miRNAs with the progression of liver fibrosis and evaluated their clinical applicability as biomarkers. Methods: This study prospectively enrolled 71 patients who underwent liver biopsy at an academic hospital in Korea. Exosomes were extracted from serum samples, followed by next-generation sequencing (NGS) of miRNAs and targeted real-time quantitative polymerase chain reaction. A model was derived to discriminate advanced fibrosis based on miRNA levels and the performance of this model was evaluated. Validation of the effect of miRNA on liver fibrosis in vitro was followed. Methods: This study prospectively enrolled 71 patients who underwent liver biopsy at an academic hospital in Korea. Exosomes were extracted from serum samples, followed by next-generation sequencing (NGS) of miRNAs and targeted real-time quantitative polymerase chain reaction. A model was derived to discriminate advanced fibrosis based on miRNA levels and the performance of this model was evaluated. Validation of the effect of miRNA on liver fibrosis in vitro was followed. Results: NGS data revealed that exosomal miR-660-5p, miR-125a-5p, and miR-122 expression were changed significantly with the progression of liver fibrosis, of which miR-122 exhibited high read counts enough to be used as a biomarker. The level of exosomal miR-122 decreased as the pathologic fibrosis grade progressed and patients with biopsy-proven advanced fibrosis had significantly lower levels of exosomal miR-122 (P < 0.001) than those without advanced fibrosis. Exosomal miR-122 exhibited a fair performance in discriminating advanced fibrosis especially in combination with fibrosis-4 score and transient elastography. In a subgroup of patients with a non-viral etiology of liver disease, the performance of exosomal miR-122 as a biomarker was greatly improved. Inhibition of miR-122 expression increased the proliferation of the human hepatic stellate cell line, LX-2, and upregulated the expression of various fibrosis related proteins. Conclusion: Exosomal miR-122 may serve as a useful non-invasive biomarker for liver fibrosis, especially in patients with non-viral etiologies of chronic liver disease.
2021-07-15 | GSE179961 | GEO
Project description:Excessive neutrophil infiltration can exacerbate inflammation and tissue damage, contributing to conditions like autoimmune disorders and liver diseases. Mesenchymal stromal cells (MSCs) share homing mechanisms with neutrophils, showing promise for treating such diseases. However, ex vivo expanded MSCs often suffer from reduced homing efficiency due to the loss of essential ligands. Here, we engineer MSCs with P-selectin and E-selectin targeting peptides, assembling them into bispecific polyvalent structures using DNA self-assembly technology. This modification allows engineered MSCs to compete with chemotactic neutrophils for selectin binding sites on endothelial cells. In a mouse model of acute liver failure, engineered MSCs effectively home to the damaged liver and significantly inhibit excessive neutrophil infiltration. The combination of inhibiting neutrophil infiltration and the MSCs’ inherent therapeutic properties lead to superior therapeutic outcomes. Single cell RNA sequencing reveals that engineered MSCs elevate the levels of Marco_macrophage which possess neutrophil-inhibitory effects. Our study offers a perspective for advancing MSC-based therapies in tissue repair.
2025-02-24 | GSE286317 | GEO