Similar Datasets
Project description:Analysis of the global gene expression in VEGF-B transgenic rat hearts
| PRJNA167973 | ENA
Project description:We examined miRNAs expression profiles in rat hearts. The expression of five of 350 scanned miRNAs significantly differed between rat hearts exposed to vehicle and diabetic rat hearts. The expression of 31 miRNAs significantly differed between vehicle and diabetes with fluctuations in glucose levels, and that of 22 miRNAs significantly differed between diabetic hearts and diabetic hearts with glucose fluctuations.
2015-11-17 | GSE40779 | GEO
Project description:We show that an excess of VEGF-B protects the heart via adaptive cardiac hypertrophy and increased coronary arterial reserve, and by inducing a shift from lipid to glucose metabolism. Six VEGF-B overexpressing transgenic hearts were compared to six littermate wildtype controls
2013-11-30 | E-GEOD-38454 | biostudies-arrayexpress
Project description:We show that an excess of VEGF-B protects the heart via adaptive cardiac hypertrophy and increased coronary arterial reserve, and by inducing a shift from lipid to glucose metabolism. Six hearts transduced with AAV-VEGF-B were compared to six AAV-HSA (human serum albumin) controls
2013-11-30 | E-GEOD-38455 | biostudies-arrayexpress
Project description:Objectives: This study aimed to determine the transcriptional basis of functional silencing of one of the two dominant pacemakers in failing rat hearts. Background: Recently, our laboratory presented functional and molecular evidence for the presence of two competing sinoatrial node (SAN) pacemakers in the healthy human and rat hearts. Anatomically localized near the superior vena cava and inferior vena cava, the superior and inferior SANs (sSAN and iSAN), respectively, preferentially control fast and slow normal heart rates. However, only one dominant pacemaker, primarily sSAN, was functional in the failing rat heart with hypertrophic cardiomyopathy. Methods: Ascending aortic constriction was performed on 1-week-old male Sprague-Dawley rat pups to induce left ventricular hypertrophy and heart failure. The dominant pacemaker was anatomically mapped in adult (8-12 weeks old) healthy and failing rat hearts using optical mapping in isolated right atrial tissue preparations. RNA sequencing was used to identify regional sSAN/iSAN gene expression differences between healthy and failing rat hearts. Results: In all failing rat hearts optically mapped in this study (n=4), only the sSAN pacemaker was functional, while the iSAN was silent. Compared to healthy rat hearts, a total of 3,640 genes were downregulated and 4,518 genes were upregulated in failing rat hearts. The functional quiescence of the iSAN in these failing rat hearts may be explained by their downregulation of sodium, potassium, and calcium ion channels as well as their downregulation of certain structural genes, including ankyrin, titin, and myosin heavy chain. Moreover, the iSAN showed predominant downregulation of several key transcription factors such as TBX5, TBX3, SHOX2, and SMAD9. Conclusions: Pressure-overload-induced heart failure resulted in significant downregulation of critical transcription factors, ion channels, and structural transcripts of the iSAN, which could explain the functional silencing of the iSAN in failing rat hearts.
2022-05-17 | GSE201717 | GEO
Project description:Differentially expressed miRNAs and mRNAs after dexmedetomidine administration in rat hearts were successfully identified by conducting microarray analysis.
2019-02-11 | GSE126105 | GEO
Project description:By combining Nkx2.5-Cre x diphtheria toxin ablation (DTA) and interspecies blastocyst complementation we have generated rat hearts into mouse embryos at E10.5. These hearts have been compared by single cell-RNA sequencing with the hearts of stage matched E11.5 rat embryo. All heart specific cell types were found in complemented chimeras, and they showed high correlation with the control. This suggests that the mechanisms of formation of the heart are compatible between mouse and rat, and that all cardiac cell types are specified correctly in the rat-to-mouse chimeras. However, global gene expression comparison identified some genes differentially expressed between complemented chimeras and control. Notably, the most relevant transcriptomic differences between rPSCs-derived hearts and rat embryonic hearts were associated with metabolism, specifically, with a decrease in oxidative phosphorylation and an increase in glycolysis processes in the rPSCs-derived cells of chimeras. Additionally, vascular endothelial cells of the complemented chimeras augmented the expression of genes related to vasculogenesis and vascular development. These changes are suggestive of a low level of oxygen in the embryo.
2023-09-20 | GSE236400 | GEO
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:Analysis of the global gene expression in the rat hearts transduced with adeno-associated viral vectors coding VEGF-B
| PRJNA167974 | ENA