ArticleJournal of molecular and cellular cardiology2009
Transcriptional remodeling of rapidly stimulated HL-1 atrial myocytes exhibits concordance with human atrial fibrillation.
Article in Journal of molecular and cellular cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- PAD2 disturbs cardiomyocyte calcium homeostasis by citrullinating SERCA2a protein in hemorrhagic shock induced arrhythmia.The journal of trauma and acute care surgery · 2025Article
- Integrative Machine Learning Analysis of Programmed Cell Death Pathways Identifies Novel Diagnostic Biomarkers for Atrial Fibrillation.Journal of inflammation research · 2025Article
- Identification of the optimal reference genes for atrial fibrillation model established by iPSC-derived atrial myocytes.BMC genomics · 2024Article
- Inhibition of the voltage-gated potassium channel Kv1.5 by hydrogen sulfide attenuates remodeling through S-nitrosylation-mediated signaling.Communications biology · 2023Article
- Natriuretic Peptide Oligomers Cause Proarrhythmic Metabolic and Electrophysiological Effects in Atrial Myocytes.Circulation. Arrhythmia and electrophysiology · 2022Article
- Fibroblast Growth Factor 21 Protects Against Atrial Remodeling via Reducing Oxidative Stress.Frontiers in cardiovascular medicine · 2021Article
- Aldehyde Dehydrogenase 2 Ameliorates Chronic Alcohol Consumption-Induced Atrial Fibrillation through Detoxification of 4-HNE.International journal of molecular sciences · 2020Article
- MulticellularFrontiers in cardiovascular medicine · 2020Review
- Lamin A mutation impairs interaction with nucleoporin NUP155 and disrupts nucleocytoplasmic transport in atrial fibrillation.Human mutation · 2019Article
- Rapid Atrial Pacing Promotes Atrial Fibrillation Substrate in Unanesthetized Instrumented Rats.Frontiers in physiology · 2019Article
- Azithromycin Causes a Novel Proarrhythmic Syndrome.Circulation. Arrhythmia and electrophysiology · 2017Article
- Association evidence of CCTTT repeat polymorphism in the iNOS promoter and the risk of atrial fibrillation in Taiwanese.Scientific reports · 2017Article
- MMP9 Rs3918242 Polymorphism Affects Tachycardia-Induced MMP9 Expression in Cultured Atrial-Derived Myocytes but Is Not a Risk Factor for Atrial Fibrillation among the Taiwanese.International journal of molecular sciences · 2016Article
- Article
- Reactive γ-ketoaldehydes promote protein misfolding and preamyloid oligomer formation in rapidly-activated atrial cells.Journal of molecular and cellular cardiology · 2015Article
- Functional and pharmacological analysis of cardiomyocytes differentiated from human peripheral blood mononuclear-derived pluripotent stem cells.Stem cell reports · 2014Article
- Quantitative Imaging of Preamyloid Oligomers, a Novel Structural Abnormality, in Human Atrial Samples.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2014Article
- Microsatellite polymorphism in the heme oxygenase-1 gene promoter and the risk of atrial fibrillation in Taiwanese.PloS one · 2014Article
- Overexpression of ryanodine receptor type 1 enhances mitochondrial fragmentation and Ca2+-induced ATP production in cardiac H9c2 myoblasts.American journal of physiology. Heart and circulatory physiology · 2013Article
- Small heat shock proteins in redox metabolism: implications for cardiovascular diseases.The international journal of biochemistry & cell biology · 2012Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
During atrial fibrillation (AF), rapid stimulation causes atrial remodeling that increases arrhythmia susceptibility. Using an established atrial (HL-1) myocyte model, we investigated the transcriptional profile associated with early atrial myocyte remodeling. Spontaneously contracting HL-1 cells were cultured in the absence and presence of rapid stimulation for 24 h and RNA harvested for microarray analysis. We identified 758 genes that were significantly altered with rapid stimulation (626 up- and 132 down-regulated). Results were confirmed using real-time quantitative RT-PCR for selected genes based on physiological relevance in human AF and/or experimental atrial tachycardia (AT), and regulation in the microarray results. In some cases, transcriptional changes were rapid, occurring within 3 h. For a selected group of genes, results were validated for the expressed protein, with findings that correlated with observed transcriptional changes. Significantly regulated genes were classified using the Gene Ontology Database to permit direct comparison of our findings with previously published myocardial transcriptional profiles. For broad functional categories, there was strong concordance between rapidly stimulated HL-1 myocytes and human AF, but not for other remodeling paradigms (cardiomyopathy and exercise). Many individual gene changes were conserved with AF/AT, with marked up-regulation of genes encoding brain and atrial natriuretic peptide precursors, and heat shock proteins. For the conserved genes, both a cellular stress and survival response was evident. Our results demonstrate similarities with human AF/experimental AT with respect to large-scale patterns of transcriptional remodeling, as well as regulation of specific individual genes. Importantly, we identified novel pathways and molecules that were concordantly regulated in vivo.
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Registered trials
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