Stable methylation loci are associated with systolic blood pressure in a Croatian island population
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PROVIDER: PRJNA857698 | ENA |
REPOSITORIES: ENA
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Project description:Adriatic islanders have a high prevalence of metabolic syndrome that is not fully explained by previous behavioral, dietary, and genetic studies. Some DNA methylation remains stable and may be established in early life, whereas others are dynamic and may vary over time in response to different conditions. The objective of the present study was to identify stable and dynamic DNA methylation loci associated with cardiometabolic traits among the populations from the island of Hvar, the largest island in the eastern Adriatic coast. An epigenome-wide association study (EWAS) was conducted using peripheral blood that was longitudinally collected at two time points, 10 years apart. DNA methylation was analyzed via Infinium MethylationEPIC BeadArray. Stable and dynamic loci were identified using linear mixed models. A total of 43,041 loci were classified as stable, while 45,769 loci were classified as dynamic. Associations between various cardiometabolic traits and stable and dynamic methylation loci were respectively assessed using linear mixed effects models adjusted for age, sex, and smoking status. After adjustment for false-discovery rate, 24 CpG loci were significantly associated with systolic blood pressure (Q < 0.1), of which 22 were stable loci and 2 were dynamic loci; while 12/22 (55%) of the systolic blood-pressure-associated stable loci resided in a gene promoter. Additionally, there was one stable locus associated with serum calcium and one with C-reactive protein. The results suggest that multiple genes involved in the determination of systolic blood pressure may be regulated via epigenetic programming established in early life.
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Project description:Full Title: Transition from Compensated Hypertrophy to Systolic Heart Failure in the Spontaneously Hypertensive Rat: Structure, Function, and Transcript Analysis Gene expression changes and left ventricular remodeling associated with the transition to systolic heart failure (HF) were determined in the spontaneously hypertensive rat (SHR). By combining transcriptomics of left ventricles from six SHR with HF with changes in function and structure we aimed to better understand the molecular events underlying the onset of systolic HF compared to six age-matched, SHR with compensated hypertrophy. Left ventricle (LV) ejection fraction was depressed (82±4 to 52±3 %) in compensated vs. failing animals. Systolic blood pressure decreased and LV end-diastolic and systolic volume increased with HF. Failing SHR hearts also demonstrated increases in left and right ventricular mass relative to non-failing SHRs.  LV papillary muscle force development and shortening velocity decreased, β-adrenergic responsiveness was depressed, myocardial stiffness and myocardial fibrosis increased with HF relative to non-failing animals. Initial micro-array analysis revealed that 1,431 transcripts were differentially expressed with HF compared to non-failing SHR (p<0.05). Of the identified transcripts, lipopolysaccharide binding protein, the most highly expressed transcript with HF, was negatively correlated to myocardial force while elevated expression of the collagen cross-linking enzyme lysyl oxidase correlated positively with muscle stiffness. Besides these individual transcripts, gene set enrichment analysis (GSEA) identified multiple enriched pathways with HF, most prominent of the altered signaling pathways involved TGF-β and insulin signaling. GESA analysis additionally identified altered gene sets involving inflammation, oxidative stress, cell degradation and cell death, among others (all p<0.01). In contrast to diastolic HF where few transcripts are reported to be altered, our data indicate multiple genes and pathways involved in a variety of biological processes characterize the onset of systolic HF, consistent with many functional and structural changes present in the failing hypertensive heart. Comprehensive gene expression profiling of heart failure Rat model vs control.
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Project description:Full Title: Transition from Compensated Hypertrophy to Systolic Heart Failure in the Spontaneously Hypertensive Rat: Structure, Function, and Transcript Analysis Gene expression changes and left ventricular remodeling associated with the transition to systolic heart failure (HF) were determined in the spontaneously hypertensive rat (SHR). By combining transcriptomics of left ventricles from six SHR with HF with changes in function and structure we aimed to better understand the molecular events underlying the onset of systolic HF compared to six age-matched, SHR with compensated hypertrophy. Left ventricle (LV) ejection fraction was depressed (82±4 to 52±3 %) in compensated vs. failing animals. Systolic blood pressure decreased and LV end-diastolic and systolic volume increased with HF. Failing SHR hearts also demonstrated increases in left and right ventricular mass relative to non-failing SHRs. LV papillary muscle force development and shortening velocity decreased, β-adrenergic responsiveness was depressed, myocardial stiffness and myocardial fibrosis increased with HF relative to non-failing animals. Initial micro-array analysis revealed that 1,431 transcripts were differentially expressed with HF compared to non-failing SHR (p<0.05). Of the identified transcripts, lipopolysaccharide binding protein, the most highly expressed transcript with HF, was negatively correlated to myocardial force while elevated expression of the collagen cross-linking enzyme lysyl oxidase correlated positively with muscle stiffness. Besides these individual transcripts, gene set enrichment analysis (GSEA) identified multiple enriched pathways with HF, most prominent of the altered signaling pathways involved TGF-β and insulin signaling. GESA analysis additionally identified altered gene sets involving inflammation, oxidative stress, cell degradation and cell death, among others (all p<0.01). In contrast to diastolic HF where few transcripts are reported to be altered, our data indicate multiple genes and pathways involved in a variety of biological processes characterize the onset of systolic HF, consistent with many functional and structural changes present in the failing hypertensive heart.
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Project description:We tested the hypothesis that a set of differentially expressed genes could be used to predict cardiovascular phenotype in mice after prolonged catecholamine stress. Experiment Overall Design: We observed that WT FVB and B2KO mice developed systolic dysfunction in response to continuous catecholamine infusion while WT C57 mice developed diastolic dysfunction. Using these mice as the derivation cohort, we identified a set of 83 genes whose differential expression correlated with left ventricle systolic dysfunction. The gene set was then used to accurately predict development of left ventricle systolic dysfunction in a separate group of mice (WT B6129SF2/J) after catecholamine stress.
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