Comprehensive analysis of the expression profiles of lncRNAs in a mouse model of alcoholic liver disease
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ABSTRACT:
PROVIDER: PRJNA733771 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14689777_1.fastq.gz | Fastqsanger.gz | |||
| SRR14689777_2.fastq.gz | Fastqsanger.gz | |||
| SRR14689778_1.fastq.gz | Fastqsanger.gz | |||
| SRR14689778_2.fastq.gz | Fastqsanger.gz | |||
| SRR14689779_1.fastq.gz | Fastqsanger.gz |
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Project description:Background and Aim: The worldwide prevalence of alcoholic liver disease (ALD) due to escalating alcohol consumption has presented an unprecedented pressure on human health. A few studies have determined long non-coding RNAs (lncRNAs) involved in the pathogenesis of liver diseases. However, the roles of lncRNAs in ALD development is still poorly understood. Methods: An ALD mouse model was established and confirmed. Expression profiles of lncRNAs were obtained by whole transcriptome sequencing. The altered lncRNAs in ALD mice were further verified by qRT-PCR. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were used to enrich the functions of these lncRNAs. In combination with miRNA and mRNA profiles, we constructed concise endogenous RNA (ceRNA) networks. The function of the most up/downregulated lnRNA signaling was further verified and investigated in both ALD model and AML-12 cells. Results: Totally, five downregulated lncRNAs were obtained and verified in ALD mice. The GO term and KEGG pathway analyses revealed that the identified lncRNAs were associated with alcohol-induced hepatic oxidative damage, cellular inflammation, and lipid metabolism. Integration the differentially modulated miRNAs and mRNAs with ceRNA network analysis, we constructed five ceRNA networks and screened out 30 miRNAs and 25 mRNAs that may participate in ALD. Further, we verified and investigate the function of the most downregulated lnc_1700023H06Rik. Depletion lnc_1700023H06Rik reduced genes related to lipid metabolism, especially mRNA Acat2 (ENSMUST00000159697) and Pgrmc2 (ENSMUST00000058578) in both ALD mice and AML12 cell. Knocking down lnc_1700023H06Rik induced triglyceride accumulation and LDH leakage in AML12 cells, consisting with that in alcohol-treated cells, confirming the potential pathological role of lnc_1700023H06Rik in ALD. Conclusion: The five remarkably downregulated lncRNAs in an ALD mouse model were identified as novel biomarkers, highlighting the key role of lncRNAs in the development of ALD. The effect of lnc_1700023H06Rik was further verified.
2021-08-18 | GSE179648 | GEO
Project description:Background and Aim: The worldwide prevalence of alcoholic liver disease (ALD) due to escalating alcohol consumption has presented an unprecedented pressure on human health. A few studies have determined long non-coding RNAs (lncRNAs) involved in the pathogenesis of liver diseases. However, the roles of lncRNAs in ALD development is still poorly understood. Methods: An ALD mouse model was established and confirmed. Expression profiles of lncRNAs were obtained by whole transcriptome sequencing. The altered lncRNAs in ALD mice were further verified by qRT-PCR. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were used to enrich the functions of these lncRNAs. In combination with miRNA and mRNA profiles, we constructed concise endogenous RNA (ceRNA) networks. The function of the most up/downregulated lnRNA signaling was further verified and investigated in both ALD model and AML-12 cells. Results: Totally, five downregulated lncRNAs were obtained and verified in ALD mice. The GO term and KEGG pathway analyses revealed that the identified lncRNAs were associated with alcohol-induced hepatic oxidative damage, cellular inflammation, and lipid metabolism. Integration the differentially modulated miRNAs and mRNAs with ceRNA network analysis, we constructed five ceRNA networks and screened out 30 miRNAs and 25 mRNAs that may participate in ALD. Further, we verified and investigate the function of the most downregulated lnc_1700023H06Rik. Depletion lnc_1700023H06Rik reduced genes related to lipid metabolism, especially mRNA Acat2 (ENSMUST00000159697) and Pgrmc2 (ENSMUST00000058578) in both ALD mice and AML12 cell. Knocking down lnc_1700023H06Rik induced triglyceride accumulation and LDH leakage in AML12 cells, consisting with that in alcohol-treated cells, confirming the potential pathological role of lnc_1700023H06Rik in ALD. Conclusion: The five remarkably downregulated lncRNAs in an ALD mouse model were identified as novel biomarkers, highlighting the key role of lncRNAs in the development of ALD. The effect of lnc_1700023H06Rik was further verified.
2021-08-18 | GSE175804 | GEO
Project description:Comprehensive analysis of the expression profiles of lncRNAs in a mouse model of alcoholic liver disease
| PRJNA744473 | ENA
Project description:Background and Aim: The worldwide prevalence of alcoholic liver disease (ALD) due to escalating alcohol consumption has presented an unprecedented pressure on human health. A few studies have determined long non-coding RNAs (lncRNAs) involved in the pathogenesis of liver diseases. However, the roles of lncRNAs in ALD development is still poorly understood. Methods: An ALD mouse model was established and confirmed. Expression profiles of lncRNAs were obtained by whole transcriptome sequencing. The altered lncRNAs in ALD mice were further verified by qRT-PCR. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were used to enrich the functions of these lncRNAs. In combination with miRNA and mRNA profiles, we constructed concise endogenous RNA (ceRNA) networks. The function of the most up/downregulated lnRNA was further verified and investigated in both ALD model and AML-12 cells. Results: Totally, five downregulated lncRNAs were obtained and verified in ALD mice. The GO term and KEGG pathway analyses revealed that the identified lncRNAs were associated with alcohol-induced hepatic oxidative damage, cellular inflammation, and lipid metabolism. Combination the differentially modulated miRNAs and mRNAs with ceRNA network analysis, we constructed five ceRNA networks and obtained 30 miRNAs and 25 mRNAs that may participate in ALD. Further, we verified and investigate the function of the most downregulated lnc_1700023H06Rik. Depletion lnc_1700023H06Rik reduced genes encoding for lipid metabolism, especially mRNA Acat2 (ENSMUST00000159697) and Pgrmc2 (ENSMUST00000058578) both in vivo and in vitro. Knocking down lnc_1700023H06Rik induced triglyceride accumulation and lactate dehydrogenase leakage in AML12 cells, consisting with that in alcohol-treated cells. Conclusion: The five remarkably downregulated lncRNAs in ALD mouse model were identified as novel biomarkers, highlighting the key role of lncRNAs in the development of ALD. The effect of lnc_1700023H06Rik plays a pivotal role in lipid deposition and its pathological pathway in ALD needs further investigation.
| S-EPMC8358650 | biostudies-literature
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
Project description:Non-coding RNAs (ncRNAs), including piwi-interacting RNA (piRNAs), circular RNAs (circRNAs) and long ncRNAs (lncRNAs), have been recently emerged as key regulators of pathological process of metabolic diseases. Since previous studies have reported that piRNAs and circRNAs involve in non-alcoholic fatty liver disease (NAFLD), this study was designed to explore more potential regulators of lncRNAs in NAFLD. A NAFLD mouse model was successfully constructed by providing high-fat diet (HFD) for 16 weeks as determined by immunohistology and serology assay. The lncRNAs expression profile including 549 upregulated lncRNAs and 108 downregulated lncRNAs was observed using microarray analysis, which was further confirmed by quantitative real-time Polymerase Chain Reaction (qRT-PCR). Moreover, we identified 308 differentially expressed mRNAs in the NAFLD group. Importantly, the sphingolipid signaling pathway may be significantly enriched pathways closely related to NAFLD using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Further study revealed that lncRNAs and their interacting mRNAs may participate in the pathophysiological process of NAFLD by regulating sphingolipid signaling pathway. Taken together, the current study demonstrated more potential regulators of lncRNAs and the interacting pathways between lncRNAs and mRNAs, which may provide new insights into the pathogenesis of NAFLD.
2022-05-03 | GSE202035 | GEO
Project description:Global gene expression patterns of 2 human steatosis and 9 human non-alcoholic steatohepatitis (NASH) together with their respective control patterns were analyzed to define the non-alcoholic fatty liver disease (NAFLD) progression molecular characteristics and to define NASH early markers from steatosis. Human liver samples of steatosis and non-alcoholic steatohepatitis were selected for RNA extraction and hybridization on Affymetrix microarrays. This dataset is part of the TransQST collection.
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Project description:LC-MS/MS quantitative liver proteomics for alcoholic liver disease
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Project description:Non‑alcoholic fatty liver disease (NAFLD) is the most common fatty liver disease in developed countries, in which fat accumulation in the liver is induced by non‑alcoholic factors. The present study was conducted to identify NAFLD‑associated long non‑coding RNAs (lncRNAs), mRNAs and microRNAs (miRNAs). The microarray dataset GSE72756, which included 5 NAFLD liver tissues and 5 controls, was acquired from the Gene Expression Omnibus database. Differentially expressed lncRNAs (DE‑lncRNAs) and mRNAs (DE‑mRNAs) were detected using the pheatmap package. Using the clusterProfiler package and Cytoscape software, enrichment and protein‑protein interaction (PPI) network analyses were conducted to evaluate the DE‑mRNAs. Next, the miRNA‑lncRNA‑mRNA interaction network was visualized using Cytoscape software. Additionally, RP11‑279F6.1 and AC004540.4 expression levels were analyzed by reverse transcription quantitative polymerase chain reaction. There were 318 DE‑lncRNAs and 609 DE‑mRNAs identified in the NAFLD tissues compared with the normal tissues. Jun proto‑oncogene, AP‑1 transcription factor subunit (JUN), which is regulated by AC004540.4 and RP11‑279F6.1, exhibited higher degree compared with other nodes in the PPI network. Furthermore, miR‑409‑3p and miR‑139 (targeting JUN) were predicted as PPI network nodes. In the miRNA‑lncRNA‑mRNA network, miR‑20a and B‑cell lymphoma 2‑like 11 (BCL2L11) were among the top 10 nodes. Additionally, BCL2L11, AC004540.4 and RP11‑279F6.1 were targeted by miR‑20a, miR‑409‑3p and miR‑139 in the miRNA‑lncRNA‑mRNA network, respectively. RP11‑279F6.1 and AC004540.4 expression was markedly enhanced in NAFLD liver tissues. These key RNAs may be involved in the pathogenic mechanisms of NAFLD.
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