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Phospholamban Antisense Oligonucleotides Improve Cardiac Function in Murine Cardiomyopathy

ABSTRACT: Phospholamban Antisense Oligonucleotides Improve Cardiac Function in Murine Cardiomyopathy

PROVIDER: PRJNA634911 | ENA |

REPOSITORIES: ENA

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			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

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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.

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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

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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

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

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Targeting Smyd3 by antisense oligonucleotides attenuates liver tumor growth

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

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Recruiting Endogenous ADARs with Antisense Oligonucleotides to Reprogram the Transcriptome

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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.

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Transcription profiling of Xenopus laevis early gastrulation embryos injected with antisense oligonucleotides against TBP, TLF or TBP2

Project description:Xenopus laevis embryos were injected with antisense oligonucleotides against TBP, TLF or TBP2. Embryos were allowed to develop up to stage 7 (non-injected control embryos) or stage 10.5 (early gastrula, control and antisense injected embryos) and subsequently collected for RNA and protein isolation. The transcriptome profile of antisense injected and control embryos was compared.

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