Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA232301 | ENA |
REPOSITORIES: ENA
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Project description:Reactivation of fetal gene expression patterns has been demonstrated to play a crucial role in common cardiac diseases in adult life including left ventricular (LV) hypertrophy (LVH). Thus, increased wall stress and neurohumoral activation are discussed to induce the return to expression of fetal genes after birth in LVH. We therefore aimed to test whether fetal gene expression programs are linked to the genetic predisposition to LVH. We performed genome-wide gene expression analysis by microarray-technology in a genetic rat model of LVH, i.e. the stroke-prone spontaneously hypertensive rat (SHRSP), to identify differences in expression patterns between day 20 of development (E20) and week 14 in comparison to a normotensive rat strain with low LV mass, i.e. Fischer (F344). 15232 probes from LV RNA from rats at week 14 and at E20 were detected as expressed (p < 0.05) and screened for differential expression. We identified 24 genes with a SHRSP specific up-regulation and 21 genes up-regulated in F344. Further bioinformatic analysis presented Efcab6, Ephx2 and Kcne1 as candidate genes for LVH that showed only in the hypertensive SHRSP rat a differential expression pattern during development and were significantly differentially expressed in adult SHRSP rats compared with two F344 and normotensive Wistar-Kyoto rats. They represent thus interesting novel targets for further functional analyses and the elucidation of mechanisms leading to LVH. Here we report a new approach to identify candidate genes for cardiac hypertrophy by analysing both gene expression differences between strains with contrasting cardiac phenotype and additionally the gene expression program during development. 26 samples for analysis; no replicates
2014-07-01 | E-GEOD-53512 | biostudies-arrayexpress
Project description:Reactivation of fetal gene expression patterns has been demonstrated to play a crucial role in common cardiac diseases in adult life including left ventricular (LV) hypertrophy (LVH). Thus, increased wall stress and neurohumoral activation are discussed to induce the return to expression of fetal genes after birth in LVH. We therefore aimed to test whether fetal gene expression programs are linked to the genetic predisposition to LVH. We performed genome-wide gene expression analysis by microarray-technology in a genetic rat model of LVH, i.e. the stroke-prone spontaneously hypertensive rat (SHRSP), to identify differences in expression patterns between day 20 of development (E20) and week 14 in comparison to a normotensive rat strain with low LV mass, i.e. Fischer (F344). 15232 probes from LV RNA from rats at week 14 and at E20 were detected as expressed (p < 0.05) and screened for differential expression. We identified 24 genes with a SHRSP specific up-regulation and 21 genes up-regulated in F344. Further bioinformatic analysis presented Efcab6, Ephx2 and Kcne1 as candidate genes for LVH that showed only in the hypertensive SHRSP rat a differential expression pattern during development and were significantly differentially expressed in adult SHRSP rats compared with two F344 and normotensive Wistar-Kyoto rats. They represent thus interesting novel targets for further functional analyses and the elucidation of mechanisms leading to LVH. Here we report a new approach to identify candidate genes for cardiac hypertrophy by analysing both gene expression differences between strains with contrasting cardiac phenotype and additionally the gene expression program during development.
2014-07-01 | GSE53512 | GEO
Project description:: The adult heart develops hypertrophy to reduce ventricular wall stress and maintain cardiac function in response to an increased workload. Although pathological hypertrophy generally progresses to heart failure, physiological hypertrophy may be cardioprotective. Cardiac-specific overexpression of the lipid-droplet protein perilipin 5 (Plin5) promotes cardiac hypertrophy, but it is unclear if this response is beneficial. We analyzed human RNA-sequencing data from the left ventricle and showed that cardiac PLIN5 expression correlates with upregulation of cardiac contraction-related processes. To investigate how elevated cardiac Plin5 levels affect cardiac contractility, we generated mice with cardiac-specific overexpression of Plin5 (MHC-Plin5 mice). These mice displayed increased left ventricular mass and cardiomyocyte size but preserved heart function. Quantitative proteomics identified sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2 (SERCA2) as a Plin5-interacting protein. Phosphorylation of phospholamban, the master regulator of SERCA2, was increased in MHC-Plin5 versus wild-type cardiomyocytes. Live imaging showed increases in intracellular Ca2+ release during contraction, Ca2+ removal during relaxation, and SERCA2 function in MHC-Plin5 versus wild-type cardiomyocytes. These results identify a role for Plin5 in improving cardiac contractility through enhanced Ca2+ signaling.
2023-01-20 | PXD035121 | Pride
Project description:To identify novel targets in left ventricular (LV) hypertrophy (LVH) we initiated comparative transcriptome analysis between genetic models derived from stroke-prone spontaneously hypertensive rats (SHRSP) and Fischer (F344). Previous genetic studies in the SHRSP/F344 model confirmed the presence of a major quantitative trait locus (QTL) for LV mass on rat chromosome (RNO) 1. We assigned carboxypeptidase X 2 (Cpxm2) to a genetic locus for LV mass identified in SHRSP. We assigned carboxypeptidase X 2 (Cpxm2) to a genetic locus for left ventricular mass.
2023-07-10 | GSE154326 | GEO
Project description:Cardiac left ventricular physiological hypertrophy in swine
| PRJNA165671 | ENA
Project description:The spontaneously hypertensive rat (SHR) is the most widely used model of essential hypertension and is predisposed to left ventricular hypertrophy, myocardial fibrosis, and metabolic disturbances. Recently, a quantitative trait locus (QTL) influencing blood pressure, left ventricular mass and heart interstitial fibrosis was genetically isolated within 788 kb on chromosome 8 segment of SHR-PD5 congenic strain that contains only 7 genes, including mutant Plzf (promyelocytic leukemia zinc finger) gene. To identify Plzf as a quantitative trait gene, we targeted Plzf in the SHR using the TALEN technique and obtained SHR line harboring mutant Plzf gene with a premature stop codon at position of amino acid 58. The Plzf mutant allele is semi-lethal since approximately 95% of newborn homozygous animals die perinatally due to multiple developmental abnormalities. Heterozygous rats were grossly normal and were used for metabolic and hemodynamic analyses. SHR-Plzf+/- heterozygotes versus SHR wild type controls exhibited reduced body weight and relative weight of epididymal fat, lower serum and liver triglycerides and cholesterol and better glucose tolerance. In addition, SHR-Plzf+/- rats exhibited significantly increased sensitivity of adipose and muscle tissue to insulin action when compared to wild type controls. Blood pressure was comparable in SHR versus SHR-Plzf+/-, however, there was significant amelioration of cardiomyocyte hypertrophy and cardiac fibrosis in SHR-Plzf+/- rats. Gene expression profiles in the liver and expression of selected genes in the heart revealed differentially expressed genes playing a role in metabolic pathways, PPAR signaling, and cell cycle regulation. These results provide evidence for an important role of Plzf in regulation of metabolic and cardiac traits in the rat and suggest a cross-talk between cell cycle regulators, metabolism, cardiac hypertrophy and fibrosis.
2016-07-03 | E-MTAB-3831 | biostudies-arrayexpress
Project description:Cardiac hypertrophy has been well-characterized at the level of transcription. During cardiac hypertrophy, genes normally expressed primarily during fetal heart development are re-expressed, and this fetal gene program is believed to be a critical component of the hypertrophic process. Recently, alternative splicing of mRNA transcripts has been shown to be temporally regulated during heart development, leading us to consider whether fetal patterns of splicing also reappear during hypertrophy.We hypothesized that patterns of alternative splicing occurring during heart development are recapitulated during cardiac hypertrophy. Here we present a whole-transcriptome study of isoform expression during pressure-overload cardiac hypertrophy induced by 10 days of transverse aortic constriction (TAC) in rats and in developing fetal rat hearts compared to sham-operated adult rat hearts, using high-throughput sequencing of poly(A) tail mRNA. Quantification of isoform expression in fetal rat hearts, pressure-overloaded rat hearts, and sham-operated rat hearts by Illumina GAIIx in triplicate
2013-05-14 | E-GEOD-42411 | biostudies-arrayexpress
Project description:Cardiac hypertrophy has been well-characterized at the level of transcription. During cardiac hypertrophy, genes normally expressed primarily during fetal heart development are re-expressed, and this fetal gene program is believed to be a critical component of the hypertrophic process. Recently, alternative splicing of mRNA transcripts has been shown to be temporally regulated during heart development, leading us to consider whether fetal patterns of splicing also reappear during hypertrophy.We hypothesized that patterns of alternative splicing occurring during heart development are recapitulated during cardiac hypertrophy. Here we present a whole-transcriptome study of isoform expression during pressure-overload cardiac hypertrophy induced by 10 days of transverse aortic constriction (TAC) in rats and in developing fetal rat hearts compared to sham-operated adult rat hearts, using high-throughput sequencing of poly(A) tail mRNA.
2013-05-14 | GSE42411 | GEO
Project description:Cardiac left ventricular physiological hypertrophy in swine
2015-07-27 | E-GEOD-37922 | ExpressionAtlas
Project description:Cardiovascular disease (CVD) in chronic kidney disease (CKD) is characterized by vascular calcification and cardiac remodeling. CKD induced cardiac hypertrophy precedes cardiac fibrosis and is associated with left ventricular dysfunction. Elevated phosphate concentration due to renal failure is known to be involved in cardiac remodeling.
2016-10-25 | GSE89130 | GEO