Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of significantly differential expression of long noncoding RNAs and pathways in hepatic fibrosis rat liver issues

ABSTRACT: Objective: To identify the long noncoding (lncRNA) and its potential roles in hepatic fibrosis rat liver issues induced by CCl4. Methods: LncRNAs and genes were analyzed in fibrosis rat liver issues by RNA sequencing and verified by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Differential expressed lncRNAs and genes were subjected to bioinformatics analysis and involved to construct co-expression network.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE173085 | GEO | 2021/04/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Identification of significantly differential expression of long noncoding RNAs and pathways in hepatic fibrosis rat liver issues

Project description:Identification of significantly differential expression of long noncoding RNAs and pathways in hepatic fibrosis rat liver issues

| PRJNA723768 | ENA

Expression data that were specifically regulated by lncRNA-LFAR1 in livers of mice undergoing hepatic fibrosis.

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 the livers of mice treated with oil in combination with injection of Lenti-NC (NC, n=3), CCl4 in combination with injection of Lenti-NC (NC+CCl4, n=3), oil in combination with injection of Lenti-shLFAR1 (shLFAR1, n=3) and CCl4 in combination with injection of Lenti-shLFAR1 (shLFAR1+CCl4, n=3) by mRNA microarrays, which revealed a panel of mRNAs that were specifically regulated by lncRNA-LFAR1 in livers of mice undergoing hepatic fibrosis. To identify the roles of lncRNAs-LFAR1 in regulating liver fiboris and the potential targets of lncRNA-LFAR1 in liver fiboris,we determined the mRNA expression profiles in the livers of Balb/c mice treated with oil in combination with injection of Lenti-NC (NC, n=3), CCl4 in combination with injection of Lenti-NC (NC+CCl4, n=3), oil in combination with injection of Lenti-shLFAR1 (shLFAR1, n=3) and CCl4 in combination with injection of Lenti-shLFAR1 (shLFAR1+CCl4, n=3) by mRNA microarrays.

2016-10-26 | GSE89147 | GEO

Expression data that were specifically regulated by lncRNA-HELF (ENSMUST00000147617 ) in livers of mice undergoing CCl4-induced liver fibrosis

Project description:Long non-coding RNAs (lncRNAs) are involved in numerous biological functions and pathological processes. In this study, we have identified a novel lncRNA ENSMUST00000147617, named Highly Expressed in Liver Fibrosis (lnc-HELF), which is remarkably up-regulated in mouse and human fibrotic livers. To identify the roles of lnc-HELF in liver fibrosis, we performed RNA-seq to analyze the effect of lnc-HELF deficient on CCl4-induced liver fibrosis. The mice were divided in three groups: mice treated with CCl4 in combination with injection of AAV8-NC (NC_CCl4, n=3), mice treated with CCl4 in combination with injection of AAV8-shRNA-lncHELF1# (sh1_CCl4, n=3) and mice treated with CCl4 in combination with injection of AAV8-shRNA-lncHELF2# (sh2_CCl4, n=3).

2023-10-05 | GSE182485 | GEO

LncRNA Airn alleviates liver fibrosis and maintains LSECs differentiation via the KLF2-eNOS-sGC pathway

Project description:Long noncoding RNAs (lncRNAs) have emerged as important regulators in a variety of human diseases. It has been suggested that dysregulation of liver sinusoidal endothelial cells (LSECs) phenotype is a critical early event in the fibrotic process. However, the biological function of lncRNAs in LSECs still remains unclear. Here, we identified that lncRNA-Airn was significantly up-regulated in liver tissues and LSECs of CCl4-induced liver fibrosis. Moreover, the expression of AIRN in human cirrhotic liver tissues and serums was remarkably increased as compared with healthy controls. In vivo studies showed that Airn deficiency aggravated CCl4- and BDL-induced liver fibrosis, while Airn overexpression by adeno-associated viral vector serotype 8 vector alleviated CCl4-induced liver fibrosis. Furthermore, we revealed that Airn maintained LSECs differentiation in vivo and in vitro. Additionally, Airn inhibited hepatic stellate cells (HSCs) activation indirectly by regulating LSECs differentiation and promoted hepatocytes (HCs) proliferation by the increased paracrine secretion of Wnt2a and HGF from LSECs. Mechanistically, our results demonstrated that Airn maintained LSECs differentiation through KLF2-endothelial nitric oxide synthase (eNOS)-soluble guanylate cyclase (sGC) pathway, thereby promoting HSCs quiescence and HCs proliferation. In conclusion, our work identified that Airn is beneficial to liver fibrosis by maintaining LSECs differentiation and might be a novel serum biomarker for liver fibrogenesis.

2021-05-11 | GSE174175 | GEO

Expression data from murine fibrotic liver tissues and normal liver tissues

2016-04-25 | GSE80601 | GEO

Genome wide mapping of long noncoding (lnc) RNAs in hepatic stellate cells

Project description:Hepatic stellate cells are the primary cell type responsible for development of fibrosis in chronic liver disease. We used directional RNA sequencing (RNA-seq) and chromatin immunoprecipitation and sequencing (ChIP-seq) to identify the lncRNAs expressed in human HSCs. We also identified the lncRNAs that change in expression with differentiation of nonfibrotic quiescent HSCs into fibrotic HSC myofibroblasts and those that are regulated by TGF-beta signaling. ChIP-seq was also performed to identify DNA regions occupied by H3K27ac to define super-enhancers in HSC myofibroblasts. This study identified lncRNAs expressed HSCs that may regulate fibrosis. Analysis of genome-wide lncRNA expression using RNA-seq and ChiP-seq in human HSCs under four different conditions

2016-03-23 | E-GEOD-68108 | biostudies-arrayexpress

MiR-29a regulates liver fibrosis

Project description:To confirm the mechanism of miR-29a in liver fibrosis healing, we have employed whole genome microarray expression profiling as a discovery platform to identify genes. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been observed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis. We can get only one gene (PDGF-c) as a target of miR-29a which relate to liver fibrosis and down-regulated more than 1.5 times in common miR-29a injected group than N.C group. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been obserbed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis.

2015-03-31 | E-GEOD-67423 | biostudies-arrayexpress

Conserved long noncoding RNA TILAM promotes liver fibrosis in humans and mice.

Project description:Fibrosis is the common endpoint for all forms of chronic liver injury, and progression of fibrosis is responsible for the development of end stage liver disease and liver failure. The activation of hepatic stellate cells (HSCs) and their transition to HSC myofibroblasts is a key step in the disease process, as these cells are the primary source of the extracellular matrix (ECM) proteins, which form the fibrotic scar. Long noncoding (lnc) RNAs can regulate the activity of HSCs, and lncRNAs that promote the fibrotic activity of HSCs may provide targets for antifibrotic therapies. Here, we identified and defined the functional mechanisms of a conserved lncRNA that plays a critical role in promoting liver fibrosis. We found that TILAM is conserved between human and mouse HSCs, and regulates expression of type 1 collagen, a major component of the ECM. To determine the role of TILAM in vivo, we annotated the mouse ortholog (Tilam), generated Tilam-deficient GFP-reporter mice, and challenged these mice in two different models of liver fibrosis. Analysis of GFP expression revealed that Tilam is induced in murine HSCs with the development of fibrosis in vivo. In both male and female mice, we also observed that loss of Tilam resulted in reduced fibrosis in the setting of injury induced by carbon tetrachloride (CCl4) and choline-deficient L-amino acid defined high fat diet (CDA-HFD). Finally, we found that TILAM interacts with PML to stabilize PML protein expression and promote the fibrotic activity of HSCs. Together, these results define an lncRNA conserved between humans and mice that is activated uniquely in HSCs to drive the development of fibrosis and could provide a therapeutic target to combat the development of end stage liver disease.

2024-07-22 | GSE238159 | GEO

RNA sequencing of WT and Hmgb2-/- mice liver treated with CCL4

Project description:loss of Hmgb2 in vivo in mouse liver largely prevented CCl4-induced liver fibrosis. The goal of the RNA-seq is to identify the Hmgb2 regulated genes in CCL4 induced liver fibrosis.

2019-10-01 | GSE98577 | GEO

Project description:Liver from CCl4-induced liver fibrosis mice

| PRJNA1065942 | ENA