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Expression data that were specifically regulated by lncRNA-LFAR1 in mouse primary HSCs

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE96526 | GEO | 2017/03/14

SECONDARY ACCESSION(S): PRJNA378929

REPOSITORIES: GEO

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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 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

Genome-wide analysis of long noncoding RNA expression profile in non-alcoholic fatty liver disease

Project description:Non-alcoholic fatty liver disease (NAFLD) is a common liver disorder and affects approximately one third of the general population.Recent studies have shown that long non-coding (lncRNA) plays critical roles in a myriad of biological processes and human diseases,Since the roles of lncRNA in NAFLD remain unknown,they were investigated in the study.Our findings indicate that the expression profiles of lncRNAs has changed in NAFLD as compared with normal liver, and may provide novel insight into the molecular mechanism underlying the disease and potential novel diagnostic or therapeutic targets for NAFLD. Microarray expression profiling of mRNAs and lncRNAs were conducted using RNA extracted from five NAFLD liver tissues and five normal liver samples.

2015-09-08 | E-GEOD-72756 | biostudies-arrayexpress

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

Senescence-associated lncRNAs: senescence-associated long noncoding RNAs.

Project description:Noncoding RNAs include small transcripts, such as microRNAs and piwi-interacting RNAs, and a wide range of long noncoding RNAs (lncRNAs). Although many lncRNAs have been identified, only a small number of lncRNAs have been characterized functionally. Here, we sought to identify lncRNAs differentially expressed during replicative senescence. We compared lncRNAs expressed in proliferating, early-passage, 'young' human diploid WI-38 fibroblasts [population doubling (PDL) 20] with those expressed in senescent, late-passage, 'old' fibroblasts (PDL 52) by RNA sequencing (RNA-Seq). Numerous transcripts in all lncRNA groups (antisense lncRNAs, pseudogene-encoded lncRNAs, previously described lncRNAs and novel lncRNAs) were validated using reverse transcription (RT) and real-time, quantitative (q)PCR. Among the novel senescence-associated lncRNAs (SAL-RNAs) showing lower abundance in senescent cells, SAL-RNA1 (XLOC_023166) was found to delay senescence, because reducing SAL-RNA1 levels enhanced the appearance of phenotypic traits of senescence, including an enlarged morphology, positive Î²-galactosidase activity, and heightened p53 levels. Our results reveal that the expression of known and novel lncRNAs changes with senescence and suggests that SAL-RNAs play direct regulatory roles in this important cellular process. RNA was extracted from both young and senescent WI-38 cells and used for total RNA-Seq.

2016-02-08 | E-GEOD-77675 | biostudies-arrayexpress

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

Project description: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.

2021-04-23 | GSE173085 | GEO

Unraveling the molecular mechanism of hyperlipidemia using integrated lncRNA and mRNA microarray data

Project description:Long non-coding RNAs (lncRNAs) play key roles in various diseases; however, their functions in hyperlipidemia (HLP) are unclear. In the present study, microarray technology was utilized to analyze the differential expression of lncRNAs and mRNAs in liver tissues of HLP ApoE-/- mice and control mice. We identified 104 and 96 differentially expressed lncRNAs and mRNAs, respectively. Differentially expressed genes were significantly enriched in biological processes such as nitric oxide biosynthesis, innate immune response, and inflammatory response. Two pairs of target genes and 38 transcription factors with regulatory functions in HLP were predicted based on the lncRNA and mRNA co-expression network. The lncRNA expression profile changes significantly in liver tissues of HLP mice model, and can provide new targets for research and treatment.

2021-05-18 | GSE169398 | GEO

Dicer-microRNA-Myc circuit promotes transcription of hundreds of long noncoding RNAs

Project description:Long noncoding RNAs (lncRNAs) are important regulators of cell fate, and their mis-expression has been implicated in many diseases. While distinct polymerases generate messenger vs. noncoding ribosomal or tRNAs3, little is known about distinct mechanisms controlling lncRNA expression. Here we show that transcription of lncRNAs is quantitatively different from that of messenger RNAs (mRNAs)--as revealed by deficiency of Dicer (Dcr), a key ribonuclease that generates microRNAs (miRNAs). Loss of Dcr in mouse embryonic stem cells (mESCs) led surprisingly to decreased level of the majority of lncRNAs. The canonical Dgcr8-Dcr-miRNA pathway is required for robust lncRNA expression, at the level of transcriptional initiation and elongation of lncRNA genes rather than at the level of their stability. cMyc, an oncogenic transcription factor, whose expression is indirectly regulated by Dcr-miRNA in mESCs, is partly responsible for lncRNA transcription. Loss of cMyc led to a more dramatic decrease of lncRNAs than mRNAs, and cMyc overexpression rescues lncRNA expression in Dcr KO cells. A quantitative metric of “mRNA-lncRNA decoupling” revealed that Dcr and cMyc differentially regulate lncRNAs vs. mRNAs in diverse cell types and in vivo, as evidenced by hundreds of microarray experiments. Thus, Dcr and cMyc may allow numerous lncRNAs to be activated or deactivated as a class, implicating lncRNAs to potential regulatory roles in development and disease states where Dcr and cMyc have been associated with. RNA was sequenced from WT and Dcr KO mESCs and the expression of lncRNAs and mRNAs are compared between WT and Dcr KO mESCs.

2014-06-15 | E-GEOD-55338 | biostudies-arrayexpress

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

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