Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

LncRNA expression data from human plasma of control donors and chronic HF patients

ABSTRACT: There are a lot of non-coding RNAs in human plasma. Some of them could be a biomarker of diseases. We used microarrys to detect lncRNAs in plasma of 10 control subjects and 10 heart failure (HF) patients diagnosed with dilated cardiomyopathy (DCM) and we identified distinct classes of dysregulated lncRNAs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE124401 | GEO | 2019/01/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Distinct Circulating Expression Profiles of Long Non-coding RNAs in Heart Failure Patients with Ischemic and Non- ischemic Dilated Cardiomyopathy

Project description:Ischemic cardiomyopathy(ICM) and dilated cardiomyopathy(DCM), with distinct long-term prognosis and responses to treatment, are two major problems that lead to heart failure(HF) ultimately. In this study, we investigated the lncRNA and mRNA expressions in the plasma of patients with DCM and ICM and analyzed the different lncRNA profile between the two groups. These findings revealed for the first time the specific expression pattern of both protein-coding RNAs and lncRNAs in plasma of HF patients due to DCM and ICM which may provide some important evidence to conveniently identify the etiology of myocardial dysfunctions and help to explore a better strategy for future HF prognosis evaluation.

2022-10-08 | GSE138678 | GEO

Expression signature of cardiac muscle as a potential diagnostic or prognostic tool for dilated cardiomyopathy

Project description:There is an emerging hypothesis that dilated cardiomyopathy (DCM) is a manifestation of end-stage heart failure (ESHF) resulting from “final common pathway” despite heterogeneous primary etiologies. We performed genome-wide expression profiling by means of high-density oligonucleotide microarrays using cardiac muscles from patients with DCM or specific cardiomyopathy as well as non-disease control hearts. Differentially expressed genes between ESHF and non-disease samples should include both genes reactive to heart failure (HF) and those responsible for ESHF. With the aid of samples with acute HF without DCM and those with DCM without HF (corrected with left ventricular assist device), we successfully distinguished ESHF genes from HF genes. Our findings implicate that transcriptional signature of cardiac muscle can be potentially applied as a diagnostic or prognostic tool for severe HF. Keywords: disease state analysis

2008-01-09 | GSE9800 | GEO

Ehrlichia sp. HF strain:HF

Project description:Ehrlichia sp. HF strain:HF Genome sequencing

| PRJNA187357 | ENA

Differential expression of microRNAs and their target genes in Dilated Cardiomyopathy

Project description:We aimed to identify aberrantly expressed microRNA and mRNA expression profiles of dilated cardiomyopathy (DCM) and explore their potential functions, 10 DCM blood samples and paired healthy control blood samples underwent RNA-sequence.

2019-09-24 | GSE117841 | GEO

Expression profiling of long noncoding RNAs and mRNAs in mouse heart, whole blood (WB), and plasma.

Project description:Long noncoding RNA profile in the heart, whole blood, and plasma before and heart failure (HF). In the study presented here, we mixed the five pairs of mouse hearts, whole blood, and plasma before and after HF and identified the genome-wide expression level of lncRNAs.

2013-11-12 | E-GEOD-48885 | biostudies-arrayexpress

Phospholamban Antisense Oligonucleotides Improve Cardiac Function in Murine Cardiomyopathy

Project description:Heart failure (HF) is a major cause of morbidity and mortality worldwide, but therapeutic intervention remains limited despite recent improvements. Aberrant Ca2+ handling is a key feature of HF pathophysiology. Restoring the Ca2+ regulating machinery is an attractive therapeutic strategy supported by genetic and pharmacological proof of concept studies. Here, we studied antisense oligonucleotides (ASOs) as a novel therapeutic modality, interfering with the PLN/SERCA2a interaction by targeting Pln mRNA for downregulation in the heart of murine HF models. Mice harboring the PLN R14del pathogenic variant recapitulate the human dilated cardiomyopathy (DCM) phenotype; subcutaneously administrated PLN-ASO prevented PLN protein aggregation, cardiac dysfunction, and led to a 3-fold increase in survival rate. In another genetic DCM mouse model, unrelated to PLN (as a disease driver) (Cspr3/Mlp-/-), PLN-ASO also reversed the HF phenotype. Finally, in rats with myocardial infarction, progression of left ventricular dilatation was prevented by PLN-ASO treatment, which also improved left ventricular contractility. Thus, our data establish PLN-ASO as a possible precision medicine for genetic cardiomyopathy as well as general HF.

2021-06-11 | GSE151156 | GEO

Sex differences during acute myocarditis against coxsackievirus B3 (CVB3)-induced myocarditis (10 dpi) and chronic myocarditis/dilated cardiomyopathy (DCM) against CVB3-induced myocarditis (90 dpi)

Project description:Men are at an increased risk of dying from heart failure caused by inflammatory heart diseases such as atherosclerosis, myocarditis and dilated cardiomyopathy (DCM). We previously showed that immune responses in the heart are phenotypically distinct in male compared to female mice 10 days after infection resulting in severe DCM in males.

2012-01-19 | GSE35182 | GEO

LncRNA expression data from human plasma of control donors and chronic HF patients

Project description:LncRNA expression data from human plasma of control donors and chronic HF patients

| PRJNA511952 | ENA

Enhancing Cardiac Cell Proliferation and Survival Suppresses Dilated Cardiomyopathy caused by Ttn-insufficiency

Project description:Dilated cardiomyopathy (DCM), defined by left ventricular (LV) enlargement associated with impaired cardiac performance, is a major cause of heart failure (HF). This results in a dilated, thin-walled left ventricle that fails to supply sufficient blood to the body. Truncating variants in TTN (TTNtv), coding for the largest structural protein in the sarcomere, contribute to the largest portion of familial and ambulatory DCM. The mechanisms for how TTNtv lead to cardiac dilation are unclear. Here, we show that reduction of Ttn expression by shRNA (Ttn shRNA) generated DCM in both mouse and rat. Ttn shRNA transduced mice developed typical DCM manifestations including impaired cardiac performance, enlarged LV and reduced LV wall thickness. Gene profiling indicates cardiac metabolism, cell proliferation and survival related genes are significantly dysregulated in Ttn shRNA-induced DCM. TUNEL assay showed Ttn shRNA induced a significant increase of cardiac cell apoptosis. A screen of 15 dysregulated downstream genes identified candidates, including Esrra, Esrrb and Yy1 significantly suppressed Ttn shRNA-induced cardiac dilation and/or DCM. Ttn shRNA induced cardiac cell apoptosis was ameliorated by Yy1. Importantly, by inducing D-type cyclin, Yy1 initiated cardiomyocyte cell cycle reentry facilitating the restoration of cardiac performance. Our findings demonstrate that DCM caused by Ttn insufficiency can be treated by therapeutically enhancing cardiac cell proliferation and survival.

2020-03-26 | GSE112319 | GEO

Proteomic analysis of donor and cardiomyopathy pre-mortem human hearts

Project description:Our understanding of heart failure (HF) has been provided by indirect surrogates, such as post-mortem histology, cardiovascular imaging, and molecular characterisation in vivo and in vitro, rather than directly in pre-mortem human cardiac tissue. Using our heart bank of pre-mortem hearts procured according to the most stringent protocols, we examined ischemic (ICM) and dilated cardiomyopathy (DCM) -- the most common causes of HF and leading causes of cardiac transplantation1. We performed unbiased, comprehensive, paired proteomic and metabolomic analysis of 51 left ventricular (LV) samples from 44 cryopreserved pre-mortem human ICM and DCM hearts, including age-matched, healthy, histopathologically-normal donor controls of both genders for comparison. Data integration via pathway and correlation network analysis revealed overlapping and divergent disease pathways in ICM and DCM, and, strikingly, precise sex-specific differences within each disease that unveil the interaction of gender with HF. Identified core functional nodes in each disease may serve as novel therapeutic targets, and we provide all proteomic and metabolomic results via an interactive online repository (https://mengboli.shinyapps.io/heartomics/) as a publicly available resource.

2023-05-18 | PXD014826 | Pride

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