Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

HL-1 cardiomyocyte response to hypoxia

ABSTRACT: Expression profiling of cultured HL-1 cardiomyocytes subjected to hypoxia for 8 hours. Three samples from each condition were analyzed

ORGANISM(S): Mus musculus

SUBMITTER: Jeanna Perman

PROVIDER: E-GEOD-27975 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction.

Perman Jeanna C JC Boström Pontus P Lindbom Malin M Lidberg Ulf U StÅhlman Marcus M Hägg Daniel D Lindskog Henrik H Scharin Täng Margareta M Omerovic Elmir E Mattsson Hultén Lillemor L Jeppsson Anders A Petursson Petur P Herlitz Johan J Olivecrona Gunilla G Strickland Dudley K DK Ekroos Kim K Olofsson Sven-Olof SO Borén Jan J

The Journal of clinical investigation 20110613 7

Impaired cardiac function is associated with myocardial triglyceride accumulation, but it is not clear how the lipids accumulate or whether this accumulation is detrimental. Here we show that hypoxia/ischemia-induced accumulation of lipids in HL-1 cardiomyocytes and mouse hearts is dependent on expression of the VLDL receptor (VLDLR). Hypoxia-induced VLDLR expression in HL-1 cells was dependent on HIF-1α through its interaction with a hypoxia-responsive element in the Vldlr promoter, and VLDLR p ...[more]

PMID: 21670500

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Project description:Atrial fibrillation (AF) is a progressive arrhythmia for which current therapy is inadequate. During AF, rapid stimulation causes atrial remodeling that promotes further AF. The cellular signals that trigger this process remain poorly understood, however, and elucidation of these factors would likely identify new therapeutic targets. We have previously shown that immortalized mouse atrial (HL-1) myocytes subjected to 24 hr of rapid stimulation in culture undergo remodeling similar to that seen in animal models of atrial tachycardia (AT) and human AF. This preparation is devoid of confounding in vivo variables that can modulate gene expression (e.g., hemodynamics). Therefore, we investigated the transcriptional profile associated with early atrial cell remodeling. RNA was harvested from HL-1 cells cultured for 24 hr in the absence and presence of rapid stimulation and subjected to microarray analysis. Data were normalized using Robust Multichip Analysis (RMA), and genes exhibiting significant differential expression were identified using the Significance Analysis of Microarrays (SAM) method. Using this approach, 919 genes were identified that were significantly altered with rapid stimulation (763 up-regulated and 156 down-regulated). For many individual transcripts, changes typical of AF/AT were observed, with marked up-regulation of genes encoding BNP and ANP precursors, heat shock proteins, and MAP kinases, while novel signaling pathways and molecules were also identified. Both stress and survival response were evident, as well as up-regulation of multiple transcription factors. Genes were also functionally classified based on cellular component, biologic process, and molecular function using the Gene Ontology database to permit direct comparison of our data with other gene sets regulated in human AF and experimental AT. For broad categories of genes grouped by functional classification, there was striking conservation between rapidly stimulated HL-1 cells and AF/AT. Results were confirmed using real-time quantitative RT-PCR on 13 genes selected by physiological relevance in AF/AT and regulation in the microarray analysis (up, down, and nonregulated). Rapidly-stimulated atrial myocytes provide a complementary experimental paradigm to explore the initial cellular signals in AT remodeling to identify novel targets in the treatment of AF. Experiment Overall Design: HL-1 cell expression profile in vitro with and without rapid electric stimulation

Dataset Information

HL-1 cardiomyocyte response to hypoxia

Publications

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction.

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