Gene expression profile of cells from Hey2 enhancer-LacZ transgenic (Tg) mouse embryos at embryonic day (E) 7.5.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE227506 | GEO | 2023/09/07
REPOSITORIES: GEO
Similar Datasets
Project description:We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy. To determine the role of CHF1/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium. We found that both wild type and transgenic mice developed increased ventricular weight to body weight ratios one week after aortic banding. Wild type mice also developed decreased fractional shortening after one week when compared to preoperative echocardiograms and sham operated controls. Transgenic mice, in comparison, demonstrated preserved fractional shortening. Histological examination of explanted heart tissue demonstrated extensive fibrosis in wild type hearts, but minimal fibrosis in transgenic hearts. TUNEL staining demonstrated increased apoptosis in the wild type hearts but not in the transgenic hearts. Exposure of cultured neonatal myocytes from wild type and transgenic animals to hydrogen peroxide, a potent inducer of apoptosis, demonstrated increased apoptosis in the wild type cells. Gene Set Analysis of microarray data from wild type and transgenic hearts one week after banding revealed suppression and activation of multiple pathways involving apoptosis, cell signaling and biosynthesis. These findings demonstrate that CHF1/Hey2 promotes physiological over pathological hypertrophy in pressure overload through suppression of apoptosis and global regulation of multiple transcriptional pathways. Experiment Overall Design: Ascending aortic banding on four wild type and four transgenic mice were compared
2010-02-17 | E-GEOD-13031 | biostudies-arrayexpress
Project description:As Grl/Hey2 directly binds DNA through E box motifs and mediates transcription repression, we aim to gain insights into potential target genes of Grl/Hey2 during heart regeneration. We performed RNA-seq analyses using total RNAs collected from 4-HT-treated Tg(cmlc2:creER;cmlc2:nRSGG) hearts and Tg(cmlc2:nRSGG) control hearts, as well as grl5nt-/- mutant hearts and wild-type hearts following ventricular resection at 7 dpa. Using RNA profile analyses, we have identified some potential genes act downstream of Grl/Hey2-dependent transcriptional repression during heart regeneration.
2020-09-14 | GSE129499 | GEO
Project description:Background: We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy and promotes physiological hypertrophy in an aortic banding model. To identify transcriptional pathways regulated by CHF1/Hey2 in hypertrophy, we cultured primary neonatal mouse cardiac myocytes from wild type and transgenic mice overexpressing CHF1/Hey2 and treated them with serum, a potent hypertrophic stimulus. We determined transcriptional profiles by hybridization to Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays. We identified important biological processes regulated by CHF1/Hey2 by Gene Set Analysis using Biological Process Gene Sets from the Gene Ontology Consortium. Results: We found that overexpression of CHF1/Hey2 suppresses gene sets involved in water transport, regulation of adenylate cyclase activity, embryonic eye morphogenesis, gut development and fluid transport after serum stimulation. Genes involved in protein dephosphorylation, in contrast, demonstrate increased expression in myocytes overexpressing CHF1/Hey2, and this increase is independent of serum treatment. Genes overexpressed prior to serum treatment are involved in regulation of transcription factor activity, protein export from the nucleus, and steroid hormone receptor signaling. Genes overexpressed after serum treatment are involved in autophagy, apoptosis and mitochondrial biogenesis. Conclusions: CHF1/Hey2 suppresses fluid transport, activation of adenylate cyclase activity, promotes phosphatase activity, autophagy and regulates other important biological processes likely relevant to hypertrophy.
2010-01-04 | GSE14288 | GEO
Project description:Background: We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy and promotes physiological hypertrophy in an aortic banding model. To identify transcriptional pathways regulated by CHF1/Hey2 in hypertrophy, we cultured primary neonatal mouse cardiac myocytes from wild type and transgenic mice overexpressing CHF1/Hey2 and treated them with serum, a potent hypertrophic stimulus. We determined transcriptional profiles by hybridization to Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays. We identified important biological processes regulated by CHF1/Hey2 by Gene Set Analysis using Biological Process Gene Sets from the Gene Ontology Consortium. Results: We found that overexpression of CHF1/Hey2 suppresses gene sets involved in water transport, regulation of adenylate cyclase activity, embryonic eye morphogenesis, gut development and fluid transport after serum stimulation. Genes involved in protein dephosphorylation, in contrast, demonstrate increased expression in myocytes overexpressing CHF1/Hey2, and this increase is independent of serum treatment. Genes overexpressed prior to serum treatment are involved in regulation of transcription factor activity, protein export from the nucleus, and steroid hormone receptor signaling. Genes overexpressed after serum treatment are involved in autophagy, apoptosis and mitochondrial biogenesis. Conclusions: CHF1/Hey2 suppresses fluid transport, activation of adenylate cyclase activity, promotes phosphatase activity, autophagy and regulates other important biological processes likely relevant to hypertrophy. Transgenic Mice and Neonatal Mouse Myocyte Culture: WT no serum, 5; WT with serum, 7; TG no serum, 6; TG with serum, 7.
2010-04-08 | E-GEOD-14288 | biostudies-arrayexpress
Project description:We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy. To determine the role of CHF1/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium. We found that both wild type and transgenic mice developed increased ventricular weight to body weight ratios one week after aortic banding. Wild type mice also developed decreased fractional shortening after one week when compared to preoperative echocardiograms and sham operated controls. Transgenic mice, in comparison, demonstrated preserved fractional shortening. Histological examination of explanted heart tissue demonstrated extensive fibrosis in wild type hearts, but minimal fibrosis in transgenic hearts. TUNEL staining demonstrated increased apoptosis in the wild type hearts but not in the transgenic hearts. Exposure of cultured neonatal myocytes from wild type and transgenic animals to hydrogen peroxide, a potent inducer of apoptosis, demonstrated increased apoptosis in the wild type cells. Gene Set Analysis of microarray data from wild type and transgenic hearts one week after banding revealed suppression and activation of multiple pathways involving apoptosis, cell signaling and biosynthesis. These findings demonstrate that CHF1/Hey2 promotes physiological over pathological hypertrophy in pressure overload through suppression of apoptosis and global regulation of multiple transcriptional pathways.
2010-01-20 | GSE13031 | GEO
Project description:RNA-sequencing of Rreb1+/+ and Rreb1-/- embryonic day 7.5 mouse embryos
2021-04-21 | GSE148514 | GEO
Project description:The cardiovascular restricted transcription factor CHF1/Hey2 has been previously shown to regulate the smooth muscle response to growth factors. To determine how CHF1/Hey2 affects the smooth muscle response to growth factors, we performed a genomic screen for transcripts that are differentially expressed in wild type and knockout smooth muscle cells after stimulation with platelet derived growth factor. We screened 45101 probes representing more than 39,000 transcripts derived from at least 34,000 genes, at eight different time points. We analyzed the expression data utilizing an algorithm based on Bayesian statistics to derive the best polynomial clustering model to fit the expression data. We found that in a total of 9827 transcripts the normalized ratio of knockout to wild type expression diverged more than 3 fold from baseline in at least one time point, and these transcripts separated into 17 distinct clusters. Further analysis of each cluster revealed distinct alterations in gene expression patterns for immediate early genes, transcription factors, matrix metalloproteinases, signaling molecules and other molecules important in vascular biology. Keywords: time course
2007-03-01 | GSE6526 | GEO
Project description: Not available
| S-EPMC3635834 | biostudies-literature
Project description:The cardiovascular restricted transcription factor CHF1/Hey2 has been previously shown to regulate the smooth muscle response to growth factors. To determine how CHF1/Hey2 affects the smooth muscle response to growth factors, we performed a genomic screen for transcripts that are differentially expressed in wild type and knockout smooth muscle cells after stimulation with platelet derived growth factor. We screened 45101 probes representing more than 39,000 transcripts derived from at least 34,000 genes, at eight different time points. We analyzed the expression data utilizing an algorithm based on Bayesian statistics to derive the best polynomial clustering model to fit the expression data. We found that in a total of 9827 transcripts the normalized ratio of knockout to wild type expression diverged more than 3 fold from baseline in at least one time point, and these transcripts separated into 17 distinct clusters. Further analysis of each cluster revealed distinct alterations in gene expression patterns for immediate early genes, transcription factors, matrix metalloproteinases, signaling molecules and other molecules important in vascular biology. Experiment Overall Design: WT and Hey2 knockout mouse aortic smooth muscle cells were treated in parallel with PDGF and harvested at successive time points for RNA extraction and hybridization on Affymetrix microarrays. We sought to identify differentially expressed transcripts through Bayesian statistical methods that would explain the differential response to PDGF observed in vitro.
2007-11-15 | E-GEOD-6526 | biostudies-arrayexpress
Project description: Not available
| S-EPMC3008721 | biostudies-literature