ArticleThe Biochemical journal2012
Feedback regulation by Atf3 in the endothelin-1-responsive transcriptome of cardiomyocytes: Egr1 is a principal Atf3 target.
Article in The Biochemical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
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- Integrating Single-Cell RNA-Seq and ATAC-Seq Analysis Reveals Uterine Cell Heterogeneity and Regulatory Networks Linked to Pimpled Eggs in Chickens.International journal of molecular sciences · 2024Article
- Pulmonary Hypertension Induced by Right Pulmonary Artery Occlusion: Hemodynamic Consequences ofJournal of the American Heart Association · 2024Article
- Adaptive transcriptomic and immune infiltrate responses in the tumor immune microenvironment following neoadjuvant chemotherapy in high grade serous ovarian cancer reveal novel prognostic associations and activation of pro-tumorigenic pathways.Frontiers in immunology · 2022Article
- Commonalities of optic nerve injury and glaucoma-induced neurodegeneration: Insights from transcriptome-wide studies.Experimental eye research · 2021Review
- Ring finger protein 2 promotes colorectal cancer progression by suppressing early growth response 1.Aging · 2020Article
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- Cyclooxygenase (COX) Inhibition by Acetyl Salicylic Acid (ASA) Enhances Antitumor Effects of Nitric Oxide in Glioblastoma In Vitro.Molecular neurobiology · 2019Article
- Boolean Modeling Reveals the Necessity of Transcriptional Regulation for Bistability in PC12 Cell Differentiation.Frontiers in genetics · 2016Article
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- Data mining reveals a network of early-response genes as a consensus signature of drug-induced in vitro and in vivo toxicity.The pharmacogenomics journal · 2014Article
- Modelling negative feedback networks for activating transcription factor 3 predicts a dominant role for miRNAs in immediate early gene regulation.PLoS computational biology · 2014Article
- Transcriptional profiling of mammary gland in Holstein cows with extremely different milk protein and fat percentage using RNA sequencing.BMC genomics · 2014Article
- Characterization of the regulatory mechanisms of activating transcription factor 3 by hypertrophic stimuli in rat cardiomyocytes.PloS one · 2014Article
- Gene expression profiles in engineered cardiac tissues respond to mechanical loading and inhibition of tyrosine kinases.Physiological reports · 2013Article
- Loss of SUMOylation on ATF3 inhibits proliferation of prostate cancer cells by modulating CCND1/2 activity.International journal of molecular sciences · 2013Article
- p90 ribosomal S6 kinases play a significant role in early gene regulation in the cardiomyocyte response to G(q)-protein-coupled receptor stimuli, endothelin-1 and α(1)-adrenergic receptor agonists.The Biochemical journal · 2013Article
- Adult cardiac expression of the activating transcription factor 3, ATF3, promotes ventricular hypertrophy.PloS one · 2013Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Endothelin-1 promotes cardiomyocyte hypertrophy by inducing changes in gene expression. Immediate early genes including Atf3 (activating transcription factor 3), Egr1 (early growth response 1) and Ptgs2 (prostaglandin-endoperoxide synthase 2) are rapidly and transiently up-regulated by endothelin-1 in cardiomyocytes. Atf3 regulates the expression of downstream genes and is implicated in negative feedback regulation of other immediate early genes. To identify Atf3-regulated genes, we knocked down Atf3 expression in cardiomyocytes exposed to endothelin-1 and used microarrays to interrogate the transcriptomic effects. The expression of 23 mRNAs (including Egr1 and Ptgs2) was enhanced and the expression of 25 mRNAs was inhibited by Atf3 knockdown. Using quantitative PCR, we determined that knockdown of Atf3 had little effect on up-regulation of Egr1 mRNA over 30 min, but abolished the subsequent decline, causing sustained Egr1 mRNA expression and enhanced protein expression. This resulted from direct binding of Atf3 to the Egr1 promoter. Mathematical modelling established that Atf3 can suffice to suppress Egr1 expression. Given the widespread co-regulation of Atf3 with Egr1, we suggest that the Atf3-Egr1 negative feedback loop is of general significance. Loss of Atf3 caused abnormal cardiomyocyte growth, presumably resulting from the dysregulation of target genes. The results of the present study therefore identify Atf3 as a nexus in cardiomyocyte hypertrophy required to facilitate the full and proper growth response.
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