Expression data from murine cardiac tissue
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE22881 | GEO | 2011/12/31
SECONDARY ACCESSION(S): PRJNA128137
REPOSITORIES: GEO
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Project description:Gender dimorphism exists in the physiological response to diet and other environmental factors. Trans-hydrogenated fatty acid (TFA) intake is associated with an increase in coronary heart disease (CHD), and gender differences in the incidence of CHD are well documented. Neonatal administration of Monosodium Glutamate (MSG) causes stunted heart growth and hypoplasticity; and gender dimorphism at the growth hormone axis has been demonstrated in MSG-treated rodents. The identification of gender dimorphism in cardiac nutrigenomics may provide the basis for gender-specific medicine in the future. We used microarray analysis to examine changes in cardiac gene transcription in response to TFA and/or MSG feeding in male and female C57Bl/6J mice. Our study animals were bred from female C57Bl/6J mice fed a standard chow diet until 6 weeks of age whereupon they were placed on one of 4 different dietary regimens for a period of 3 weeks prior to mating. The four dietary regimens used in this study were: [1] Standard Chow (Control diet) with ad lib drinking water. [2] Standard Chow, with ad lib drinking water containing 0.64 g/L Monosodium Glutamate (MSG diet). [3] Trans fat diet of 20% (w/w) Partially Hydrogenated Vegetable Shortening containing 8.68% w/w Trans fatty acids(TFA diet). [4] Trans fat Diet #5C4M together with ad lib drinking water containing 0.64 g/L Monosodium Glutamate (TFA+MSG diet). Following mating, the 4 groups of dams were maintained on their respective diets throughout the gestation and nursing period. Male and female offspring used in the following experiments were weighed, weaned onto the same diets and maintained on their respective dietary regimens until they reached 32 weeks of age.Cardiac tissues (8 per diet group) were used at 32 weeks for RNA extraction and hybridization on Affymetrix microarrays.
2011-12-31 | E-GEOD-22881 | biostudies-arrayexpress
Project description:Our previous studies have linked Trans-fat and monosodium glutamate (MSG) to the development of Nonalcoholic Fatty Liver Disease (NAFLD). We have also shown that MSG can interact with another commonly consumed food additive, aspartame, to impair glucose homeostasis, which is also disrupted in NAFLD. This most recent nutrigenomic study shows how aspartame, MSG and Trans-fat can unfavorably alter hepatic and adipose tissue gene expression. We used microarray analysis to examine changes in adipose gene transcription in response to TFA MSG and/or ASP feeding in male C57Bl/6J mice.
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Project description:Our previous studies have linked Trans-fat and monosodium glutamate (MSG) to the development of Nonalcoholic Fatty Liver Disease (NAFLD). We have also shown that MSG can interact with another commonly consumed food additive, aspartame, to impair glucose homeostasis, which is also disrupted in NAFLD. This most recent nutrigenomic study shows how aspartame, MSG and Trans-fat can unfavorably alter hepatic and adipose tissue gene expression. We used microarray analysis to examine changes in liver gene transcription in response to TFA MSG and/or ASP feeding in male C57Bl/6J mice.
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Project description:Sexual dimorphisms are well recognized in various cardiac diseases, including myocardial infarction (MI). MI develops later in women, but once established, it contributes more persistent symptoms and higher mortality than in men. Although mRNA-level sexual dimorphism of MI have been reported, whether miRNA transcriptome also confers such dimorphism remains unknown. Comprehensive understanding of the mRNA- and miRNA-level genetic programs underlying the heart sexual dimorphisms will expectedly improve clinical outcome by facilitating the development of gender specific treatment strategies. Here, by conducting miRNA microarray analysis of human MI samples, we set out to characterize the heart sexual dimorphisms at the level of miRNA transcriptome
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Project description:The heart, the first organ to develop, undergoes complex morphogenesis that when defective results in congenital heart disease (CHD). With current therapies, more than 90% of CHD patients survive into adulthood but often suffer premature death from heart failure (HF) and non-cardiac causes 1. To gain insight into poorly understood disease progression, we performed single nuclear RNA sequencing (snRNA-seq) and analyzed more than 157,000 nuclei from donors and CHD patients, including hypoplastic left heart syndrome (HLHS) and Tetralogy of Fallot (TOF), two common forms of cyanotic CHD lesions, as well as, dilated (DCM) and hypertrophic (HCM) cardiomyopathies. We observed CHD specific cell states in cardiomyocytes (CMs) which had evidence of insulin resistance and increased FOXO and CRIM1 expression. Cardiac fibroblasts (CFs) in HLHS had enrichment for a low HIPPO and high YAP cell state characteristic of activated CFs. Imaging Mass Cytometry (IMC) uncovered the spatially resolved perivascular microenvironment consistent with an immunodeficient state in CHD. Peripheral immune cell profiling suggested deficient monocytic immunity in CHD in agreement with CHD predilection to infection and cancer 2. Our comprehensive CHD phenotyping provides a roadmap for future personalized medicine in CHD.
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Project description:Dysplasia of cardiac endothelial cells significantly contributes to congenital heart disease (CHD), the most common congenital disability. The regulatory role of miRNAs in this process remains elusive. This study identified elevated miR-187 expression in embryonic heart endothelial cells from CHD fetuses. Using a conditional knock-in model, we showed that increased miR-187 levels in embryonic endothelial cells induce CHD in homozygous fetal mice, closely mirroring human CHD. Mechanistically, miR-187 targets NIPBL, which is responsible for recruiting the cohesin complex and facilitating chromatin accessibility between enhancers and promoters. Consequently, the endothelial cell-specific upregulation of miR-187 inhibited NIPBL, leading to reduced chromatin accessibility and impaired gene expression, which hindered endothelial cell development and ultimately caused heart septal defects and reduced heart size both in vitro and in vivo. Importantly, exogenous miR-187 expression in human cardiac organoids mimicked developmental defects in the cardiac endothelial cells, reversible by NIPBL replenishment. Our findings establish the miR-187/NIPBL axis as a potent regulator that inhibits cardiac endothelial cell development by attenuating the transcription of numerous endothelial genes, with our mouse and human cardiac organoid models effectively replicating severe defects from minor perturbations.
2024-11-03 | GSE275950 | GEO
Project description:Dysplasia of cardiac endothelial cells significantly contributes to congenital heart disease (CHD), the most common congenital disability. The regulatory role of miRNAs in this process remains elusive. This study identified elevated miR-187 expression in embryonic heart endothelial cells from CHD fetuses. Using a conditional knock-in model, we showed that increased miR-187 levels in embryonic endothelial cells induce CHD in homozygous fetal mice, closely mirroring human CHD. Mechanistically, miR-187 targets NIPBL, which is responsible for recruiting the cohesin complex and facilitating chromatin accessibility between enhancers and promoters. Consequently, the endothelial cell-specific upregulation of miR-187 inhibited NIPBL, leading to reduced chromatin accessibility and impaired gene expression, which hindered endothelial cell development and ultimately caused heart septal defects and reduced heart size both in vitro and in vivo. Importantly, exogenous miR-187 expression in human cardiac organoids mimicked developmental defects in the cardiac endothelial cells, reversible by NIPBL replenishment. Our findings establish the miR-187/NIPBL axis as a potent regulator that inhibits cardiac endothelial cell development by attenuating the transcription of numerous endothelial genes, with our mouse and human cardiac organoid models effectively replicating severe defects from minor perturbations.
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