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Molecular Mediators of Cardiac Pathology in Cardiorenal Syndrome Type 4 [anti-miR-21]

ABSTRACT: We report the changes in left ventricle mRNA abundance in response to miR-21-5p suppression in 5/6 nephrectomized rats.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE98522 | GEO | 2017/05/04

SECONDARY ACCESSION(S): PRJNA385371

REPOSITORIES: GEO

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Molecular Mediators of Cardiac Pathology in Cardiorenal Syndrome Type 4

Project description:We report the changes in left ventricle mRNA and miRNA abundance in response to 5/6 nephrectomy surgery This SuperSeries is composed of the SubSeries listed below.

2017-05-04 | GSE97950 | GEO

Molecular Mediators of Cardiac Pathology in Cardiorenal Syndrome Type 4 [miRNA]

Project description:We report the changes in left ventricle miRNA abundance in response to 5/6 nephrectomy surgery

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Molecular Mediators of Cardiac Pathology in Cardiorenal Syndrome Type 4 [mRNA]

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Molecular Mediators of Cardiac Pathology in Cardiorenal Syndrome Type 4

Project description:Molecular Mediators of Cardiac Pathology in Cardiorenal Syndrome Type 4

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MicroRNA-21 regulates peroxisome proliferator-activated receptor alpha, a molecular mechanism of cardiac pathology in Cardiorenal Syndrome Type 4.

Project description:Cardiovascular events are the leading cause of death in patients with chronic kidney disease (CKD), although the pathological mechanisms are poorly understood. Here we longitudinally characterized left ventricle pathology in a 5/6 nephrectomy rat model of CKD and identify novel molecular mediators. Next-generation sequencing of left ventricle mRNA and microRNA (miRNA) was performed at physiologically distinct points in disease progression, identifying alterations in genes in numerous immune, lipid metabolism, and inflammatory pathways, as well as several miRNAs. MiRNA miR-21-5p was increased in our dataset and has been reported to regulate many identified pathways. Suppression of miR-21-5p protected rats with 5/6 nephrectomy from developing left ventricle hypertrophy and improved left ventricle function. Next-generation mRNA sequencing revealed that miR-21-5p suppression altered gene expression in peroxisome proliferator-activated receptor alpha (PPAR?) regulated pathways in the left ventricle. PPAR?, a miR-21-5p target, is the primary PPAR isoform in the heart, importantly involved in regulating fatty acid metabolism. Therapeutic delivery of low-dose PPAR? agonist (clofibrate) to rats with 5/6 nephrectomy improved cardiac function and prevented left ventricle dilation. Thus, comprehensive characterization of left ventricle molecular changes highlights the involvement of numerous signaling pathways not previously explored in CKD models and identified PPAR? as a potential therapeutic target for CKD-related cardiac dysfunction.

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Cardiorenal Effects of Peritoneal Dialysis in the 5/6Nx Uremic Rat Model

Project description:In this study we compare transcriptomic changes in the kidney and left ventricle in response to peritoneal dialyisis exchanges performed 3x per day for 8 days beginning 6 weeks after 5/6 nephrectomy or sham surgery in 10 week old male Sprague Dawley rats. .

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Mouse models of cardiac remodeling

Project description:We employed the Affymetrix GeneChip technology to evaluate the patterns of expression in two different in vivo models of cardiac remodeling and in two different regions (left ventricle free wall and septum) of the heart. Mice underwent transverse aortic constriction (TAC); myocardial infarction (MI) or Sham operation and RNA from the left ventricle free wall and the septum was isolated 1 week later. Keywords: other

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miR-21, Mediator, and Potential Therapeutic Target in the Cardiorenal Syndrome.

Project description:Oligonucleotide-based therapies are currently gaining attention as a new treatment option for relatively rare as well as common diseases such as cardiovascular disease. With the remarkable progression of new sequencing technologies, a further step towards personalized precision medicine to target a disease at a molecular level was taken. Such therapies may employ antisense oligonucleotides to modulate the expression of both protein coding and non-coding RNAs, such as microRNAs. The cardiorenal syndrome (CRS) is a complex and severe clinical condition where heart and renal dysfunction mutually affect one another. The underlying mechanisms remain largely unknown and current treatments of CRS are mainly supportive therapies which slow down the progression of the disease, but hardly improve the condition. The small non-coding RNA, microRNA-21 (miR-21), is dysregulated in various heart and kidney diseases and has been repeatedly suggested as therapeutic target for the treatment of CRS. Impressive preclinical results have been achieved by an antisense oligonucleotide-based therapy to effectively block the pro-fibrotic traits of miR-21. Since microRNA-mediated pathways are generally very well-conserved, there is considerable commercial interest with regards to clinical translation. In this review, we will summarize the role of miR-21 within the heart-kidney axis and discuss the advantages and pitfalls of miR-21 targeting therapeutic strategies in CRS.

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