Heart Rate Fragmentation in WBS
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ABSTRACT:
PROVIDER: PRJNA1037272 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: The purpose of this study was to comprehensively identify the gene expression changes that occur after chronic sleep fragmentation. Method: We conducted total microarray analysis of the heart in mice following 5 weeks of sleep fragmentation. Results: The microarray analysis revealed significant and dramatic gene expression changes in the mouse heart as a result of chronic sleep fragmentation. Conclusion: This study provides valuable insights into the biological impact of chronic sleep fragmentation, shedding light on the molecular mechanisms involved.
2024-07-31 | GSE236358 | GEO
Project description:AMP-activated protein 1 kinase (AMPK), a phylogenetically conserved serine/threonine kinase regarded as a key cellular energy sensor, exists in eukaryotes as a heterotrimer comprising a catalytic α and regulatory β and γ subunits. In humans, activating mutations in the gene encoding the γ2 subunit of AMPK (PRKAG2) display a cardiac phenotype of left ventricular hypertrophy (LVH), conduction system disease, ventricular pre-excitation and increased cardiomyocyte glycogen accumulation. While existing transgenic models have elucidated the pathogenesis of several aspects of the disease5-7, the slow heart rate (sinus bradycardia) – a prominent feature of the disease – remains poorly understood. Here, using gene-targeting to generate mice which recapitulate this bradycardia, we demonstrate that γ2 AMPK activation perturbs fundamental mechanisms that determine sinoatrial pacemaker cell function. Reduction in the sarcolemmal hyperpolarization activated (“funny”) current (If) and damping of ryanodine receptor-derived diastolic local subsarcolemmal Ca2+ releases (LCRs)12,13 contribute to reduced sinoatrial cell spontaneous activity and, ultimately, to a lower heart rate. Pharmacological activation of AMPK reversibly reduces the beating rate of murine pluripotent stem cell-derived induced sinoatrial bodies. In contrast, using a mouse knock-out of γ2 AMPK, which exhibits an increased heart rate, we demonstrate a role for γ2 AMPK in physiological heart rate regulation, including an indispensable role in the bradycardic adaptation to endurance exercise. Through regulating the cardiac pacemaker and thereby heart rate, γ2 AMPK by virtue of its energy-sensing role, is a key physiological determinant of overall cardiac energy homeostasis.
2017-09-30 | GSE73047 | GEO
Project description:Introduction: Gain-of-function (GOF) mutations in the cardiac pacemaker channel HCN4 have been associated with inappropriate sinus tachycardia in human patients. Chronic tachycardia is generally associated with adverse cardiac remodeling and cardiomyopathy, but whether enhanced HCN4 activity can induce or modulate such remodeling remains unknown. We aimed to investigate the influence of an HCN4 gain-of-function mutation on cardiac function and structure under baseline and pressure overload conditions. Methods and Results: We generated HCN4(Y527F) knock-in mice (HCN4F) carrying a GOF mutation in the C-Linker of HCN4 channels, which shifts their activation curves to more positive potentials. Electrophysiological recordings confirmed increased channel availability at physiological membrane potentials. Telemetric ECGs and in vivo electrophysiological studies revealed an elevated mean and intrinsic heart rate, faster sinus node and atrioventricular conduction in HCN4F mice, but no spontaneous arrhythmias. In HCN4F mice, the heart rate histogram was truncated at lower heart rates, indicating fewer low-rate intervals and more frequent periods of elevated heart rate, while maximal heart rates remained comparable between the two phenotypes. Histological analysis did not reveal structural changes consistent with tachycardia-induced cardiomyopathy. Cardiac morphology, fibrosis, and contractility were indistinguishable between genotypes up to 12 months of age. Following transverse aortic constriction, both WT and HCN4F mice developed left ventricular hypertrophy, but HCN4F hearts exhibited less chamber dilatation, smaller left ventricular lumen, and preserved systolic function compared to WT. Gene expression and RNA-sequencing analyses revealed activation of a typical hypertrophic gene program in both genotypes, but distinct remodeling signatures. Discussion: The HCN4(Y527F) gain-of-function mutation increases intrinsic heart rate without inducing structural or functional deterioration. Under pressure overload, it even confers protection against maladaptive dilatation and contractile dysfunction. These findings challenge the concept that persistent inappropriately elevated heart rate is necessarily detrimental and suggest that enhanced HCN4 activity may facilitate adaptive cardiac responses to stress.
2026-07-01 | GSE329403 | GEO
Project description:Chip-Seq on P0 heart-mouse (fragmentation date:2015-08-26) For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2017-01-04 | GSE92140 | GEO
Project description:Chip-Seq on P0 heart-mouse (fragmentation date:2015-08-26) For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2017-01-04 | GSE91756 | GEO
Project description:Chip-Seq on P0 heart-mouse (fragmentation date: 2015-02-05) For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2017-01-04 | GSE91494 | GEO
Project description:Recent advances in small RNA research reveal that noncanonical small RNAs, such as tRNA-derived small RNAs (tsRNAs) and rRNA-derived small RNAs (rsRNAs), are more abundant than well-known microRNAs in various tissue/cell types. Distinct fragmentation of parental RNAs (e.g., tRNA and rRNA) can generate functionally diverse small RNAs. Therefore, we propose a computational tool (qMAP) to identify differential fragmentation of parental RNAs between different biological conditions. Using qMAP, we tested aging-associated differential RNA fragmentation in mouse sperm heads between young and old mice. 28S rRNA was found to exhibit the most significant differential fragmentation. One short rsRNA candidate (17-nt) and one long rsRNA candidate (44-nt) were selected as their involvement of the observed differential fragmentation of 28S rRNA. These two candidate rsRNAs were transfected into mouse embryonic stem cells (mESCs), respectively. mRNA sequencing on these mESCs revealed a distinct transcriptomic response to the 17-nt and 44-nt rsRNAs.
2026-05-13 | GSE330870 | GEO
Project description:It remains unclear how sleep influences inflammatory pathways after myocardial infarction (SF). In this study, we relied on established murine models and assessed how sleep fragmentation (SF) alters transcriptional programing in the blood, heart, and brain after MI.
2024-10-30 | GSE275089 | GEO
Project description:qMAP decodes RNA fragmentation dynamics
| PRJNA1465826 | ENA
Project description:Interventions: experimental group:Dexmedetomidine was intravenously pumped during the operation;control group:Intraoperative intravenous infusion of the same volume of normal saline
Primary outcome(s): Heart Rate Variability
Study Design: Non randomized control
| 2694562 | ecrin-mdr-crc