Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The novel long noncoding RNA Lnc19959.2 modulating triglyceride metabolism associated genes through interaction with Purb and hnRNPA2B1

ABSTRACT: High triglycerides can lead to atherosclerotic cardiovascular disease. Long noncoding RNAs (lncRNAs) are currently consider to have vital and wide range of biological functions, but the molecular mechanism underlying TG metabolism remains poorly understood. To identify novel lncRNAs differentially expressed in rat liver with hypertriglyceridemia using transcriptome sequencing and elucidated the function role in TG metabolism. In our study, we identified a novel lncRNA, Lnc19959.2, which was highly expression in rat liver with hypertriglyceridemia. Knockdown of lnc19959.2 has profound TG lowering effects in vitro and vivo. Subsequently genome-wide analysis identified that knockdown of Lnc19959.2 caused deregulation of many genes during TG homeostasis. Further mechanism studies reveal that Lnc19959.2 specifically bound to Purb to up-regulate expression of Apoa4, while bound to hnRNPA2B1 to down-regulate the expression of Cpt1a, Tm7sf2 and Gpam, respectively. In the upstream pathway, palmitate acid up-regulated CCAAT/Enhancer-Binding Protein Beta (Cebpb) facilitates its binding to promoter region of Lnc19959.2, which resulted in significant promotion of lnc19959.2 transcriptional activity. Our findings provide novel insights into transcriptional regulation of TG homeostasis by a novel lncRNA. This newly identified lncRNA could be exploited as novel therapeutic targets for hypertriglyceridemia.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE137131 | GEO | 2020/06/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The novel long noncoding RNA Lnc19959.2 modulating triglyceride metabolism associated genes through interaction with Purb and hnRNPA2B1 [RNA-seq]

Project description:High triglycerides can lead to atherosclerotic cardiovascular disease. Long noncoding RNAs (lncRNAs) are currently consider to have vital and wide range of biological functions, but the molecular mechanism underlying TG metabolism remains poorly understood. To identify novel lncRNAs differentially expressed in rat liver with hypertriglyceridemia using transcriptome sequencing and elucidated the function role in TG metabolism. In our study, we identified a novel lncRNA, Lnc19959.2, which was highly expression in rat liver with hypertriglyceridemia. Knockdown of lnc19959.2 has profound TG lowering effects in vitro and vivo. Subsequently genome-wide analysis identified that knockdown of Lnc19959.2 caused deregulation of many genes during TG homeostasis. Further mechanism studies reveal that Lnc19959.2 specifically bound to Purb to up-regulate expression of Apoa4, while bound to hnRNPA2B1 to down-regulate the expression of Cpt1a, Tm7sf2 and Gpam, respectively. In the upstream pathway, palmitate acid up-regulated CCAAT/Enhancer-Binding Protein Beta (Cebpb) facilitates its binding to promoter region of Lnc19959.2, which resulted in significant promotion of lnc19959.2 transcriptional activity. Our findings provide novel insights into transcriptional regulation of TG homeostasis by a novel lncRNA. This newly identified lncRNA could be exploited as novel therapeutic targets for hypertriglyceridemia.

2020-06-08 | GSE137712 | GEO

The novel long noncoding RNA Lnc19959.2 modulating triglyceride metabolism associated genes through interaction with Purb and hnRNPA2B1 (RNA-seq data set)

2022-09-11 | GSE137252 | GEO

LncRNA and circRNA expression profiles of Aβ25-35-induced AD mice hippocampus treated with Tripterygium Glycoside

Project description:Tripterygium glycosides (TG) was reported to have effect of ameliorating Alzheimer's disease (AD). However, the mechanism is not clear. We aimed to investigate the lncRNAs and circRNAs expression profiles of AD treated with TG by using microarray. LncRNAs, mRNA and circRNA in 3 AD mice and 3 AD+TG mice hippocampal were detected by microarray. The most differentially expressed lncRNAs, mRNA and circRNA in AD+TG group were screened. The differentially expressed lncRNAs and circRNAs were analyzed for GO enrichment and KEGG pathway. Co-expression analysis of lncRNAs and mRNA was performed by calculating correlation coefficients. Protein-protein interaction (PPI) network analysis was performed on mRNAs using STRING. LncRNA-target-TFs network were analyzed by Network software. CircRNA-mirNA network were conducted by Cytoscape software. A total of differentially expressed 661 lncRNAs, 64 circRNAs and 503 mRNAs were detected in AD mice treated with TG. The Pou4f1, Egr2, Mag, and Nr4a1 were the hub genes in the PPI network. The KEGG results showed the mRNAs that co-expressed with lncRNAs were enriched in TNF, PI3K-Akt, and Wnt signaling pathway. lncRNA-target-TFs network analysis indicated the TFs including Cebpa, Zic2, and Rxra were the most likely to regulate the detected lncRNAs. The circRNA-miRNA interaction network indicated 275 miRNAs may bind to the 64 circRNAs. In conclusion, the findings supplied a novel perspective for AD pathogenesis. And the detected lncRNAs, mRNAs, and circRNAs might be novel therapeutics targets for AD.

2022-05-30 | GSE204817 | GEO

The transcription factor cyclic AMP–responsive element–binding protein H regulates triglyceride metabolism

Project description:Here we report that the transcription factor cyclic AMP–responsive element–binding protein H (CREB-H, encoded by CREB3L3) is required for the maintenance of normal plasma triglyceride concentrations. CREB-H–deficient mice showed hypertriglyceridemia secondary to inefficient triglyceride clearance catalyzed by lipoprotein lipase (Lpl), partly due to defective expression of the Lpl coactivators Apoc2, Apoa4 and Apoa5 and concurrent augmentation of the Lpl inhibitor Apoc3. We identified multiple nonsynonymous mutations in CREB3L3 that produced hypomorphic or nonfunctional CREB-H protein in humans with extreme hypertriglyceridemia, implying a crucial role for CREB-H in human triglyceride metabolism. Total RNAs were isolated from the liver of three WT and three Creb3l3 deficient mice after a 24-h fasting. Littermates were used. Gene expression profiles were examined using Illumina WG-6 microarray chips.

2011-06-04 | E-GEOD-29643 | biostudies-arrayexpress

Global identification of growth-related long non-coding RNAs in breast muscle of chicken

Project description:Long non-coding RNAs (lncRNAs) can have potential roles in development of tissues and organs. We selected breast muscle of fast-growing White Recessive Rock chicken (WRR) and slow-growing Xing Hua chicken (XH) to identify lncRNA transcripts by LncRNA-Seq. This study identified 21,993 novel lncRNAs. Among 7,339 differentially expressed lncRNAs, 723 up-regulated and 6,616 down-regulated lncRNAs were found in WRR compared with XH. Of them, five novel lncRNA were antisense transcripts for growth-related genes CACNA1D (unigene 14689_all), IL4I1 (unigene 15355_all), LEF-1 (unigene 19525_all) and FABP1 (unigenes 17536_all and 17537_all) respectively. Meanwhile, 12 other novel lncRNAs were found in the intron or downstream of some known growth-related genes (IGF1, IGF2BP2, IGF2BP3, CACNA1D, IL4I1, LEF-1 and FABP1). In addition, 4,043 SSRs and 200,049 SNPs were identified. Our data revealed the global lncRNA expression pattern in muscle tissue, and contributed a useful genomic resource towards studying the effects of lncRNAs in regulating chicken growth. Two RNA pool for WRR and XH strains

2014-06-24 | E-GEOD-58755 | biostudies-arrayexpress

Genome-wide identification of rat long non-coding RNAs (microarray)

Project description:In the current study, we have focused on a distinct group of non-coding elements, lncRNA, and profiled renal tissues from three different inbred rat strains. We chose the three strains S, SHR and R for the main purpose of cataloging lncRNA annotations from the most widely used rat models of cardiovascular and renal disease. Identification of lncRNAs on the rat genome by Microarray

2014-12-10 | E-GEOD-59165 | biostudies-arrayexpress

The transcription factor cyclic AMP–responsive element–binding protein H regulates triglyceride metabolism

2011-06-04 | GSE29643 | GEO

The long noncoding RNA Caren protects against heart failure via suppressing the Hint1-ATM signaling pathway

Project description:Long noncoding RNAs (lncRNAs) have potential as novel therapeutic targets in cardiac disease, but their function in heart failure (HF) is not yet fully understood. Using a gene trapping approach in mouse embryonic stem cells, we identified a novel cytoplasmic lncRNA, dubbed Caren (cardiomyocyte-enriched noncoding transcript), which was predominantly expressed in cardiomyocytes. Caren was markedly downregulated in the mouse failing heart that was subjected to transverse aortic constriction (TAC). The ablation of Caren in the mouse heart accelerated HF-related phenotypes by TAC, whereas mice overexpressing Caren (CAG-Caren Tg mice) resisted TAC-induced HF. Proteomic analysis identified histidine triad nucleotide-binding protein 1 (Hint1) as a Caren target protein, while bioinformatic analysis of proteome revealed that Caren regulates the proteins involved in mitochondrial energetics in the heart. Furthermore, we found that Caren suppressed Hint1 expression at the translational level and that Hint1 overexpression reduced mitochondrial respiration capacity. Similar to CAG-Caren Tg mice, the reduced Hint1 expression in mice exerted cardioprotective effects on TAC-induced HF, which was associated with the decreased level of ATM serine/threonine kinase phosphorylation, known to activate DNA damage responses. Overall, we identify a novel cytoplasmic lncRNA that protects against the development of HF through suppressing the Hint1-ATM signaling, which presumably maintains mitochondrial energetics and prevents the DNA damage under pathological stress.

2021-02-08 | PXD016186 | Pride

Genome-wide identification of rat long non-coding RNAs

2014-12-10 | E-GEOD-58701 | biostudies-arrayexpress

Novel long non-coding RNAs are involved in cellular response to angiotensin II signaling

Project description:Angiotensin II (AngII) is a polypeptide hormone that plays a pivotal role in the regulation of blood pressure. In vascular smooth muscle cells (VSMCs), AngII signaling results in hypertrophy, proliferation, contraction, and migration, which ultimately promote atherosclerosis and hypertensive cardiovascular diseases. Recent studies have shown that fundamental biological processes such as cell proliferation and differentiation are mediated in part by the activities of long non-protein-coding RNAs (lncRNAs). In this study, we sought to identify lncRNAs that are involved in the response to AngII-signaling. Genome-wide analysis of de novo assembled transcripts from rat vascular smooth muscle cells (VSMCs) identified novel lncRNA as well as protein-coding transcripts which have not been previously annotated. The majority of the genomic loci from which these novel transcripts are transcribed are enriched for histone H3 lysine 4 trimethylation and histone H3 lysine 36 trimethylation, two chromatin modifications that are closely associated with actively transcribed regions, further supporting these as bona fide transcripts. Compared with previously annotated rat transcripts, these novel lncRNA transcripts, on average, are shorter in length and are less abundant, consistent with reports from mice and humans. Expression analyses of transcripts from control and AngII-stimulated VSMCs reveal that AngII signaling affects the abundance of both protein-coding transcripts as well as lncRNAs transcripts. Altogether, these data provide new insights into the global effects of AngII signaling and reveal potential novel therapeutic targets for treatment of AngII-associated cardiovascular diseases. RNA-sequencing of control and AngII (3hrs)-stimulated rVSMSCs. ChIP-sequencing of H3K4me3 and H3K36me3 in control and AngII (3hrs)-stimulated rVSMCs.

2013-06-30 | E-GEOD-38056 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data