Expression data from HSCs
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE40381 | GEO | 2012/08/28
SECONDARY ACCESSION(S): PRJNA173817
REPOSITORIES: GEO
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Project description:Hepatic stellate cells (HSCs) experience phenotypic transformation, from the quiescent phenotype to the activated one, after different etiologies of liver injury. Liver fibrosis is then occurred upon the activation of HSCs. miR-16 deficiency is identified to be an important characteristic of HSCs activation. We used Affymetrix rat 230 2.0 arrays (Affymetrix, Santa Clara, U.S.A.) to uncover the global alternations of transcriptome under miR-16 restoration. We isolated quiescent hepatic stellate cells (HSCs) from adult male SD rats (normal control group) by in situ perfusion and density-gradient centrifugation. Activated HSCs were separated from rats of fibrosis model group, which were treated by 40% carbon tetrachloride (CCl4) for 8 weeks, by means of liver section, digestion and sequential centrifugation. Quiescent and activated HSCs were then divided into 4 groups at random, namely quiescent HSCs, activated HSCs, pLV-miR-16-treated HSCs and pLV-GFP-treated HSCs. The pLV-miR-16-treated group, pLV-GFP-treated group were infected with pLV-miR-16 and pLV-GFP, respectively.
2012-08-28 | E-GEOD-40381 | biostudies-arrayexpress
Project description:Hepatic stellate cells (HSCs) are considered to be the main source of extracellular matrix in liver fibrosis. During chronic liver injury HSCs become activated and transdifferentiate into pro-fibrotic myofibroblasts. This process is associated with major changes in gene expression as well as intracellular signaling and can potentially be regulated by microRNAs (miRNA). In a recent study we found miRNA-25-3p (miR-25) to be upregulated in serum of children with Cystic Fibrosis (CF) who have no evidence of liver disease, compared to children with CF liver disease and healthy individuals. In this study we investigated the role of miR-25 in HSC biology and on the development of liver disease.
2018-08-25 | GSE119022 | GEO
Project description:Hepatic stellate cells (HSCs) are the major driver of fibrosis by expressing extracellular matrices (ECM). HSCs, in the normal liver, are quiescent and activated by liver injury to become myofibroblasts that proliferate and produce ECM. It has been shown that activated HSCs can be deactivated by removal of liver insults. In order to evaluate the changes of gene expression profiles, we induced quiescent HSCs (qHSCs), activated HSCs (aHSCs) and deactivated HSCs (daHSCs) from human induced pluripotent stem cells and performed RNA-sequence analysis.
2024-05-01 | GSE251824 | GEO
Project description:The decline of hematopoietic stem cell (HSC) function upon aging contributes to senescent immune remodeling and to leukemia pathogenesis. Aged HSCs show epigenetic alterations affecting DNA methylation, histone modifications, and show a reduction in the polar distribution of histone 4 lysine 16 acetylation (H4K16ac). Here, we determined the deposition patterns of H4K16ac in young, aged and re-juvenated HSCs using ChIP-seq.
2018-09-20 | GSE120232 | GEO
Project description:Long noncoding RNAs (lncRNAs) play important roles in various biological processes; however, few have been identified that regulate hepatic stellate cells (HSCs) activation and the progression of liver fibrosis. Through a detailed analysis of the expression of lncRNAs in various tissues, we discovered the existence of a liver enriched lncRNA-LFAR1 (lncRNA-Liver Fibrosis Associated RNA1). To identify the roles of lncRNA-LFAR1 in liver fiboris, we systematically analyzed the regulation of mRNAs in primary HSCs infected with two separated lnc-LFAR1-shRNAs by RNA-seq, which revealed a panel of mRNAs that were specifically regulated by lncRNA-LFAR1 in mouse primary HSCs.
2017-03-14 | GSE96526 | GEO
Project description:Purpose: The goals of this study is to uncover the difference of transcriptomes that are essential for HSCs malignant transformation driven by miR-31-5p inhibition. Methods: GFP+-HSCs sorted from bone marrow mRNA profiles of mice receiving HSCs subjected to control RNA or miR-31-5p inhibitor treatment were generated by deep sequencing, using Illumina NovaSeq 6000 sequencer for 318 cycles.Reads that passed the Illumina quality filters were kept for the subsequent analyses. Adapters were trimmed from the reads, and reads shorter than 17 nt were discarded. The reads were mapped to the Mouse mRNA reference database using FANSe3 algorithm on Chi-Cloud NGS Analysis Platform (Chi-Biotech Co. Ltd., Shenzhen, China). Results: We use edgeR to analysis with a |log2 (FoldChange)| > 1 and p value <0.01. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to promote HSCs malignant driven by miR-31-5p inhibition. Conclusions: Our study represents the first detailed analysis of transcriptomes that promote T-cell malignant transformation driven by HTVL-1 oncogene Tax.
2023-12-29 | GSE163985 | GEO
Project description:Liver fibrosis is a manifestation of chronic liver injury. It leads to hepatic dysfunction and is a critical element in the pathogenesis of cirrhosis and hepatocellular carcinoma. The activation of hepatic stellate cells (HSC) plays a central role in liver fibrogenesis of different etiologies. To elucidate the molecular mechanism of this phenomenon, it is important to analyze the changes in gene expression that accompany the HSC activation process. In this study, we isolated quiescent and activated HSCs from control mice and mice with CCl4-induced liver fibrosis, respectively, and performed RNA sequencing to compare the differences in gene expression patterns between the two types of HSCs.
2020-04-29 | GSE149508 | GEO
Project description:Liver fibrosis is a common pathological process of various chronic liver diseases that can develop into liver cancer. MicroRNAs (miRNAs) are a king of non-coding RNA which are closely related to liver diseases. Thus, this research hope to explore the effect of miR-484 on liver fibrosis and reveal its mechanism. The miRNAs profiles were screened by microRNA sequencing and the location of miR-484 was identified by fluorescence in situ hybridization (FISH) in human liver fibrotic tissues. MiR-484 expression was detected by qRT-PCR in rat primary hepatic stellate cells (HSCs). Bioinformatics analysis and dual-luciferase reporter assay were performed to determine the target gene of miR-484. Liver fibrosis specific signatures were analyzed by qRT-PCR and western blot after miR-484 mimic/inhibitor transfection. The cell apoptosis was detected by Annexin V-FITC/PI double staining. The effect of miR-484 silencing on fibrosis in vivo was investigated in thioacetamide (TAA) induced mice model using the adeno-associated virus carrying miR-484 inhibitor. Enrichment of miR-484 was observed in human liver fibrosis tissues and activated rat primary HSCs. FISH showed that miR-484 was prominently located at fibrotic region and the cytoplasm of HSCs in human liver tissues. Dual-luciferase reporter assay verified that the homeodomain-interacting protein kinases 1 (HIPK1) was the direct target of miR-484. After transfecting miR-484 inhibitor into HSC-T6, HIPK1 were significantly up-regulated, and α-SMA, col1a1, Wnt-3a, Wnt-5a, β-catenin and p-β-catenin were down-regulated, suggesting the restrain effect of miR-484 knockdown on HSCs activation. Conversely, the results were opposite with miR-484 mimic transfection. In addition, the apoptosis of HSC-T6 altered significantly after miR-484 modulation. Moreover, adeno-associated virus carrying miR-484 inhibitor alleviated mice liver fibrosis induced by TAA. In conclusion, miR-484 knockdown ameliorates liver fibrosis by promoting the apoptosis and suppressing HSCs activation via blocking Wnt/β-catenin signaling pathway. MiR-484 and its downstream gene HIPK1 might be selected as novel therapeutic targets of liver fibrosis.
2021-12-09 | GSE190366 | GEO
Project description:Liver fibrosis is a high-morbidity and high-mortality chronic disease throughout the world without any satisfying treatment Large-conductance Ca2+- and voltage-activated K+ (Slo1, BK) channels are widely expressed in human body and important for numerous physiological processes. Previous studies have shown that BK channels are expressed in HSCs of patients with liver fibrosis and they are involved in contraction/relaxation of the HSCs To investigate the molecular mechanism of antifibrotic effect of BK channel opener rottlerin using in vivo fibrosis models. transcriptomic analyses of differential expression genes in livers from rats of vehicle, CCl4 and CCl4 combined with rottlerin treatment were for discrimination. The RNA samples were extracted from three samples of each group for microarray profiling and performed in Affymetrix Rats Genome 230 2.0 arrays for gene expression profiling analysis, which contained 31 042 probe sets. The biotinylated cRNA targets were hybridized with the microarray. After hybridization, arrays were stained in the Fluidics Station 450 and scanned on the Affymetrix Scanner 3000. The microarray experiments were performed by following the protocol of Affymetrix Inc at Shanghai Biotechnology Corporation. Under the criteria fold change > 1.5 or < 0.67, we obtained 10672 differential expressed genes (DEGs) between CCl4 and CCl4 combined with rottlerin treatment group, and the data was applied to further analysis.
2019-11-07 | GSE139994 | GEO
Project description:MicroRNAs (miRNAs) are endogenous and small non-coding RNA molecules that mediate post-transcriptional gene suppression by incomplete matches with their host mRNAs. Recent studies have highlighted that miRNAs are involved in the pathology of liver lipid metabolism, metabolic inflammation, oxidative stress, chronic liver injury, regeneration and fibrogenesis. During liver fibrosis, miRNAs are simply categorized into pro-fibrotic or anti-fibrotic miRNAs according to their expression alterations in one liver cell type especially hepatic stellate cells (HSCs). Our current study observed a miRNA, termed miR-150-5p, exhibited cell-specific expression pattern in liver fibrosis. Although the expression level of miR-150-5p in fibrotic liver tissues or hepatocytes was significantly enhanced, it was notably down-regulated in HSCs in the context of liver fibrosis. Perturbation of miR-150-5p evidently affected the cell viability of HSCs but had no obvious effect on hepatocytes. While overexpression of miR-150-5p could sensitize the apoptosis of hepatocytes in the presence of pro-apoptotic factors. Further investigations revealed that miR-150-5p mimic treatment had a larger influence on the transcriptomic stability of HSCs but a minor effect on hepatocytes. The genes related to anti-apoptosis or pro-proliferation were decreased and genes associated with pro-apoptosis or anti-proliferation were increased after miR-150-5p overexpression, which might be the potential targets of miR-150-5p overexpressed in HSCs. Collectively, our study provide a strong supporting evidence that some miRNAs may express or function in a cell-specific pattern in the backdrop of liver fibrosis.
2019-03-01 | GSE124411 | GEO