Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Phospholamban Antisense Oligonucleotides Improve Cardiac Function in Murine Cardiomyopathy

ABSTRACT: Phospholamban Antisense Oligonucleotides Improve Cardiac Function in Murine Cardiomyopathy

PROVIDER: PRJNA634911 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11843739.fastq.gz	Fastqsanger.gz
	SRR11843740.fastq.gz	Fastqsanger.gz
	SRR11843741.fastq.gz	Fastqsanger.gz
	SRR11843742.fastq.gz	Fastqsanger.gz
	SRR11843743.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

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

Phospholamban antisense oligonucleotides improve cardiac function in murine cardiomyopathy.

Project description:Heart failure (HF) is a major cause of morbidity and mortality worldwide, highlighting an urgent need for novel treatment options, 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 study antisense oligonucleotides (ASOs) as a 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; subcutaneous administration of PLN-ASO prevents PLN protein aggregation, cardiac dysfunction, and leads to a 3-fold increase in survival rate. In another genetic DCM mouse model, unrelated to PLN (Cspr3/Mlp-/-), PLN-ASO also reverses the HF phenotype. Finally, in rats with myocardial infarction, PLN-ASO treatment prevents progression of left ventricular dilatation and improves left ventricular contractility. Thus, our data establish that antisense inhibition of PLN is an effective strategy in preclinical models of genetic cardiomyopathy as well as ischemia driven HF.

| S-EPMC8405807 | biostudies-literature

Targeting Smyd3 by antisense oligonucleotides attenuates liver tumor growth

Project description:We investigated whether pharamacological inhibition of Smyd3 by antisense oligonucleotides (ASOs) can influence diethylnitrosamine (DEN)-induced liver cancer development. Our phenotypic analyses, among others, included gene expression profiling.

2020-06-24 | GSE153077 | GEO

Expression data from dosing four different antisense oligonucleotides in mice II

Project description:We used microarrays to globally profile the gene expression changes observed in liver after 3 days when dosing antisense oligonucleotides in mice

2018-04-30 | GSE100698 | GEO

Expression data from transfection of two different antisense oligonucleotides in HuH7 cells

Project description:We used microarrays to globally profile the gene expression changes observed after 24h when transfecting antisense oligonucleotides in HuH77 cells

2017-04-21 | GSE93245 | GEO

Expression data from transfection of 14 different antisense oligonucleotides in HuH7 cells

Project description:We used microarrays to globally profile the gene expression changes observed after 10h and 24h when transfecting antisense oligonucleotides in HuH7 cells

2017-04-21 | GSE93244 | GEO

Targeting Smyd3 by antisense oligonucleotides attenuates liver tumor growth

Project description:Targeting Smyd3 by antisense oligonucleotides attenuates liver tumor growth

| PRJNA641395 | ENA

Knockdown of circular RNAs using LNA-modified antisense oligonucleotides

Project description:Knockdown of circular RNAs using LNA-modified antisense oligonucleotides

| PRJNA607690 | ENA

Recruiting Endogenous ADARs with Antisense Oligonucleotides to Reprogram the Transcriptome

Project description:Recruiting Endogenous ADARs with Antisense Oligonucleotides to Reprogram the Transcriptome

| PRJNA497809 | ENA

Silencing of NFYC-AS1 by Gapmer antisense oligonucleotides and CRISPR/Cas9 TSS deletion.

Project description:NFYC-AS1 is an overlapping antisense RNA transcribed head-to-head to NFYC sense gene, encoding for the subunit C of NF-Y transcription factor, which is known as master regulator of cell cycle and proliferation in normal and tumor cells. Here we performed NFYC-AS1 silencing in lung squamous carcinoma H520 cells by Gapmer antisense oligonucleotides and CRISPR/Cas9 TSS deletion. Afterwards, we performed differentially expressed analysis and gene set enrichement analysis to investigate on NFYC-AS1 function and mechanism of action.

2024-03-08 | GSE240468 | GEO

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