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ABSTRACT:
PROVIDER: PRJNA282037 | ENA |
REPOSITORIES: ENA
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Project description:MDMA (ecstasy) is an illicit drug that stimulates monoamine neurotransmitter release and inhibits reuptake. MDMAâs acute cardiotoxicity includes tachycardia and arrhythmia which are associated with cardiomyopathy (CM). MDMA acute cardiotoxicity has been explored, but neither long-term MDMA cardiac pathological changes nor epigenetic changes have been evaluated. Microarray analyses were employed to identify cardiac gene expression changes and epigenetic DNA methylation changes. To identify permanent MDMA-induced pathogenetic changes, mice received daily 10d or 35d MDMA , or daily 10d MDMA followed by 25d saline washout (10+25d). MDMA treatment (10d) caused differentially gene expression (p<0.05, fold change >1.5), with 752 genes 558 genes following 35d MDMA, and 113 genes following 10d treatment +25d washout. Changes in MAPK and circadian rhythm gene expression were identified following 10d administration. After 35d, circadian rhythm genes (Per3, CLOCK, ARNTL, and NPAS2) remained differentially expressed. MDMA caused DNA hypermethylation and hypomethylation that was independent of gene expression; hypermethylation of genes was 71% at 10d, 68% at 35d, and 91% at 10+25d. Differential gene expression that corresponded directly with DNA methylation changes occurred in 22% of genes at 10d, 17% at 35d, and 48% at 10d+25d washout. MDMA treatment resulted in epigenetic changes in cardiac DNA methylation. Hypermethylation was the predominant effect. MDMA induced gene expression of key elements of circadian rhythm regulatory genes and suggest a fundamental mechanism for MDMA dysfunction in the heart. This study addresses how MDMA (ecstasy) affects cardiac (left ventricle) gene expression and epigenetic nuclear DNA methylation. Each sample was fluorescently labeled and hybridized to Roche Nimblegen 2.1M Deluxe Promoter Arrays.
2015-12-11 | E-GEOD-68199 | biostudies-arrayexpress
Project description:MDMA (ecstasy) is an illicit drug that stimulates monoamine neurotransmitter release and inhibits reuptake. MDMAâs acute cardiotoxicity includes tachycardia and arrhythmia which are associated with cardiomyopathy (CM). MDMA acute cardiotoxicity has been explored, but neither long-term MDMA cardiac pathological changes nor epigenetic changes have been evaluated. Microarray analyses were employed to identify cardiac gene expression changes and epigenetic DNA methylation changes. To identify permanent MDMA-induced pathogenetic changes, mice received daily 10d or 35d MDMA , or daily 10d MDMA followed by 25d saline washout (10+25d). MDMA treatment (10d) caused differentially gene expression (p<0.05, fold change >1.5), with 752 genes 558 genes following 35d MDMA, and 113 genes following 10d treatment +25d washout. Changes in MAPK and circadian rhythm gene expression were identified following 10d administration. After 35d, circadian rhythm genes (Per3, CLOCK, ARNTL, and NPAS2) remained differentially expressed. MDMA caused DNA hypermethylation and hypomethylation that was independent of gene expression; hypermethylation of genes was 71% at 10d, 68% at 35d, and 91% at 10+25d. Differential gene expression that corresponded directly with DNA methylation changes occurred in 22% of genes at 10d, 17% at 35d, and 48% at 10d+25d washout. MDMA treatment resulted in epigenetic changes in cardiac DNA methylation. Hypermethylation was the predominant effect. MDMA induced gene expression of key elements of circadian rhythm regulatory genes and suggest a fundamental mechanism for MDMA dysfunction in the heart. This study addresses how MDMA (ecstasy) affects cardiac (left ventricle) gene expression and epigenetic nuclear DNA methylation. Each sample was fluorescently labeled and hybridized to Roche Nimblegen 12X135kb MM9 Gene Expression Arrays.
2015-12-11 | E-GEOD-68175 | biostudies-arrayexpress
Project description:MDMA (ecstasy) is an illicit drug that stimulates monoamine neurotransmitter release and inhibits reuptake. MDMA’s acute cardiotoxicity includes tachycardia and arrhythmia which are associated with cardiomyopathy (CM). MDMA acute cardiotoxicity has been explored, but neither long-term MDMA cardiac pathological changes nor epigenetic changes have been evaluated. Microarray analyses were employed to identify cardiac gene expression changes and epigenetic DNA methylation changes. To identify permanent MDMA-induced pathogenetic changes, mice received daily 10d or 35d MDMA , or daily 10d MDMA followed by 25d saline washout (10+25d). MDMA treatment (10d) caused differentially gene expression (p<0.05, fold change >1.5), with 752 genes 558 genes following 35d MDMA, and 113 genes following 10d treatment +25d washout. Changes in MAPK and circadian rhythm gene expression were identified following 10d administration. After 35d, circadian rhythm genes (Per3, CLOCK, ARNTL, and NPAS2) remained differentially expressed. MDMA caused DNA hypermethylation and hypomethylation that was independent of gene expression; hypermethylation of genes was 71% at 10d, 68% at 35d, and 91% at 10+25d. Differential gene expression that corresponded directly with DNA methylation changes occurred in 22% of genes at 10d, 17% at 35d, and 48% at 10d+25d washout. MDMA treatment resulted in epigenetic changes in cardiac DNA methylation. Hypermethylation was the predominant effect. MDMA induced gene expression of key elements of circadian rhythm regulatory genes and suggest a fundamental mechanism for MDMA dysfunction in the heart. This study addresses how MDMA (ecstasy) affects cardiac (left ventricle) gene expression and epigenetic nuclear DNA methylation.
2015-12-11 | GSE68199 | GEO
Project description:MDMA (ecstasy) is an illicit drug that stimulates monoamine neurotransmitter release and inhibits reuptake. MDMA’s acute cardiotoxicity includes tachycardia and arrhythmia which are associated with cardiomyopathy (CM). MDMA acute cardiotoxicity has been explored, but neither long-term MDMA cardiac pathological changes nor epigenetic changes have been evaluated. Microarray analyses were employed to identify cardiac gene expression changes and epigenetic DNA methylation changes. To identify permanent MDMA-induced pathogenetic changes, mice received daily 10d or 35d MDMA , or daily 10d MDMA followed by 25d saline washout (10+25d). MDMA treatment (10d) caused differentially gene expression (p<0.05, fold change >1.5), with 752 genes 558 genes following 35d MDMA, and 113 genes following 10d treatment +25d washout. Changes in MAPK and circadian rhythm gene expression were identified following 10d administration. After 35d, circadian rhythm genes (Per3, CLOCK, ARNTL, and NPAS2) remained differentially expressed. MDMA caused DNA hypermethylation and hypomethylation that was independent of gene expression; hypermethylation of genes was 71% at 10d, 68% at 35d, and 91% at 10+25d. Differential gene expression that corresponded directly with DNA methylation changes occurred in 22% of genes at 10d, 17% at 35d, and 48% at 10d+25d washout. MDMA treatment resulted in epigenetic changes in cardiac DNA methylation. Hypermethylation was the predominant effect. MDMA induced gene expression of key elements of circadian rhythm regulatory genes and suggest a fundamental mechanism for MDMA dysfunction in the heart. This study addresses how MDMA (ecstasy) affects cardiac (left ventricle) gene expression and epigenetic nuclear DNA methylation.
2015-12-11 | GSE68175 | GEO
Project description:ECSTASY (MDMA) ALTERS CARDIAC GENE EXPRESSION AND DNA METHYLATION: IMPLICATIONS FOR CIRCADIAN RHYTHM DYSFUNCTION IN THE HEART (methylation)
| PRJNA282036 | ENA
Project description:ECSTASY (MDMA) ALTERS CARDIAC GENE EXPRESSION AND DNA METHYLATION: IMPLICATIONS FOR CIRCADIAN RHYTHM DYSFUNCTION IN THE HEART (expression)
| PRJNA282035 | ENA
Project description:Circadian rhythm disruption is associated with skeletal muscle dysfunction within the blind Mexican Cavefish
2023-01-13 | MSV000091062 | MassIVE
Project description:Cardiomyopathy (CM) is an intrinsic weakening of the myocardium with contractile dysfunction and congestive heart failure (CHF). CHF has been postulated to result from decreased mitochondrial energy production and oxidative stress. The effects of decreased mitochondrial oxygen consumption can also accelerate with aging, with the mitochondrial theory of aging forming the basis of this knowledge. We previously showed DNA methylation changes in human hearts with CM. This was associated with mitochondrial DNA depletion, being another molecular marker of CM. We examined the relationship between mitochondrial dysfunction and cardiac epigenetic DNA methylation changes in both young and old mice. We used genetically engineered C57Bl/6 mice transgenic for a cardiac-specific mutant of the mitochondrial polymerase (termed Y955C). Y955C mice undergo left ventricular hypertrophy (LVH) at a young age (~94 days old), and LVH decompensated to CHF at old age (~255 days old). In Y955C hearts, 95 differentially expressed genes were found, while 4,452 genes were differentially expressed in aged hearts. Moreover, cardiac DNA methylation patterns differed between Y955C (4,506 peaks with 68.5% hypomethylation) and aged hearts (73,286 peaks with 80.2% hypomethylated). Correlatively, of the 95 Y955C-dependent differentially expressed genes, 30 genes (31.6%) also displayed differential DNA methylation; in the 4,452 age dependent differentially expressed genes, 342 gene (7.7%) displayed associated DNA methylation changes. Both Y955C and aging demonstrated significant enrichment of CACGTG-associated E-box motifs in differentially methylated regions. Cardiac mitochondrial polymerase dysfunction alters nuclear DNA methylation. Furthermore, aging causes a robust change in cardiac DNA methylation that is partially associated with mitochondrial polymerase dysfunction. This study addresses how Y955C-mutated mitochondrial DNA polymerase g and aging affect cardiac (left ventricle) gene expression and epigenetic nuclear DNA methylation.
2016-05-06 | GSE72889 | GEO
Project description:Cardiomyopathy (CM) is an intrinsic weakening of the myocardium with contractile dysfunction and congestive heart failure (CHF). CHF has been postulated to result from decreased mitochondrial energy production and oxidative stress. The effects of decreased mitochondrial oxygen consumption can also accelerate with aging, with the mitochondrial theory of aging forming the basis of this knowledge. We previously showed DNA methylation changes in human hearts with CM. This was associated with mitochondrial DNA depletion, being another molecular marker of CM. We examined the relationship between mitochondrial dysfunction and cardiac epigenetic DNA methylation changes in both young and old mice. We used genetically engineered C57Bl/6 mice transgenic for a cardiac-specific mutant of the mitochondrial polymerase (termed Y955C). Y955C mice undergo left ventricular hypertrophy (LVH) at a young age (~94 days old), and LVH decompensated to CHF at old age (~255 days old). In Y955C hearts, 95 differentially expressed genes were found, while 4,452 genes were differentially expressed in aged hearts. Moreover, cardiac DNA methylation patterns differed between Y955C (4,506 peaks with 68.5% hypomethylation) and aged hearts (73,286 peaks with 80.2% hypomethylated). Correlatively, of the 95 Y955C-dependent differentially expressed genes, 30 genes (31.6%) also displayed differential DNA methylation; in the 4,452 age dependent differentially expressed genes, 342 gene (7.7%) displayed associated DNA methylation changes. Both Y955C and aging demonstrated significant enrichment of CACGTG-associated E-box motifs in differentially methylated regions. Cardiac mitochondrial polymerase dysfunction alters nuclear DNA methylation. Furthermore, aging causes a robust change in cardiac DNA methylation that is partially associated with mitochondrial polymerase dysfunction. This study addresses how Y955C-mutated mitochondrial DNA polymerase g and aging affect cardiac (left ventricle) gene expression and epigenetic nuclear DNA methylation.
2016-05-06 | GSE72888 | GEO
Project description:Heart disease is the leading cause of death in the developed world, and its comorbidities such as hypertension, diabetes, and heart failure are accompanied by major transcriptomic changes in the heart. During cardiac dysfunction, which leads to heart failure, there are global epigenetic alterations to chromatin that occur concomitantly with morphological changes in the heart in response to acute and chronic stress. These epigenetic alterations include the reversible methylation of lysine residues on histone proteins. Lysine methylation on histone H3K4 and H3K9 were among the first methylated lysine residues identified and have been linked to gene activation and silencing, respectively. However, much less is known regarding other methylated histone residues, including histone H4K20. Trimethylation of histone H4K20 has been shown to repressive gene expression, however this mark has never been examined in the heart. Here we utilized immunoblotting and mass spectrometry to quantify histone H4K20 trimethylation in three models of cardiac dysfunction. Our results show that lysine methylation at this site is regulated in a biphasic manner leading to increased H420 trimethylation during acute hypertrophic stress and decreased H4K20 trimethylation during sustained ischemic injury and cardiac dysfunction. In addition, we examined publicly available datasets to analyze enzymes that regulate H4K20 methylation and identified one demethylase (KDM7C) and two methyltransferases (KMT5A and SMYD5) which were all upregulated in heart failure patients. This is the first study to examine histone H4K20 trimethylation in the heart and to determine how this post-translational modification is differentially regulated in multiple models of cardiac disease.
2022-10-14 | PXD031617 | Pride