ArticleCardiovascular research2009
Atrial natriuretic peptide suppresses endothelin gene expression and proliferation in cardiac fibroblasts through a GATA4-dependent mechanism.
Article in Cardiovascular research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Discovery and replication of novel blood pressure genetic loci in the Women's Genome Health Study.Journal of hypertension · 2011Pooled it
- Podocyte specific knockout (KO) of the natriuretic peptide clearance receptor (NPRC) attenuates diabetic kidney disease (DKD).Physiological reports · 2026Article
- Carboxy-terminal 24-amino-acid peptide of integral membrane protein 2A is produced in the heart and stimulates atrial natriuretic peptide release.Scientific reports · 2026Article
- Relationship between protein arginine methyltransferase and cardiovascular disease (Review).Biomedical reports · 2022Review
- Emerging therapies: The potential roles SGLT2 inhibitors, GLP1 agonists, and ARNI therapy for ARNI pulmonary hypertension.Pulmonary circulation · 2022Review
- Glucagon-Like Peptide 1 and Atrial Natriuretic Peptide in a Female Mouse Model of Obstructive Pulmonary Disease.Journal of the Endocrine Society · 2020Article
- Cyclic nucleotide regulation of cardiac sympatho-vagal responsiveness.The Journal of physiology · 2016Review
- Proteasome inhibitors attenuated cholesterol-induced cardiac hypertrophy in H9c2 cells.BMB reports · 2016Article
- Natriuretic Peptides in the Regulation of Cardiovascular Physiology and Metabolic Events.Journal of the American Heart Association · 2015Review
- Atrial natriuretic peptide exerts protective action against angiotensin II-induced cardiac remodeling by attenuating inflammation via endothelin-1/endothelin receptor A cascade.Heart and vessels · 2013Article
- Megakaryocytic leukemia 1 (MKL1) ties the epigenetic machinery to hypoxia-induced transactivation of endothelin-1.Nucleic acids research · 2013Article
- Suppression of atrial natriuretic peptide/natriuretic peptide receptor-A-mediated signaling upregulates angiotensin-II-induced collagen synthesis in adult cardiac fibroblasts.Molecular and cellular biochemistry · 2013Article
- Article
- Molecular mechanisms underlying cardiac antihypertrophic and antifibrotic effects of natriuretic peptides.Journal of molecular medicine (Berlin, Germany) · 2012Review
- Serine 105 phosphorylation of transcription factor GATA4 is necessary for stress-induced cardiac hypertrophy in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Cellular Interplay between Cardiomyocytes and Nonmyocytes in Cardiac Remodeling.International journal of inflammation · 2011Article
- Regulation of blood pressure and salt homeostasis by endothelin.Physiological reviews · 2011Review
- Endothelin-1 gene regulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Review
- Atrial natriuretic peptide inhibits angiotensin II-stimulated proliferation in fetal cardiomyocytes.The Journal of physiology · 2010Article
- Limitations of conventional approaches to identify myocyte nuclei in histologic sections of the heart.American journal of physiology. Cell physiology · 2010Article
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5 authors.
Funding
Abstract
aimsAtrial natriuretic peptide (ANP) is a hormone that has both antihypertrophic and antifibrotic properties in the heart. We hypothesized that myocyte-derived ANP inhibits endothelin (ET) gene expression in fibroblasts. METHODS AND
resultsWe have investigated the mechanism(s) involved in the antiproliferative effect of ANP on cardiac fibroblasts in a cell culture model. We found that cardiac myocytes inhibited DNA synthesis in co-cultured cardiac fibroblasts as did treatment with the ET-1 antagonist BQ610. The effect of co-culture was reversed by antibody directed against ANP or the ANP receptor antagonist HS-142-1. ANP inhibited the expression of the ET-1 gene and ET-1 gene promoter activity in cultured fibroblasts. The site of the inhibition was localized to a GATA-binding site positioned between -132 and -135 upstream from the transcription start site. GATA4 expression was demonstrated in cardiac fibroblasts, GATA4 bound the ET-1 promoter both in vitro and in vivo, and siRNA-mediated knockdown of GATA4 inhibited ET-1 expression. ET-1 treatment resulted in increased levels of phospho-serine(105) GATA4 in cardiac fibroblasts and this induction was partially suppressed by co-treatment with ANP.
conclusionCollectively, these findings suggest that locally produced ET-1 serves as an autocrine stimulator of fibroblast proliferation, that ANP produced in neighbouring myocytes serves as a paracrine inhibitor of this proliferation, and that the latter effect operates through a reduction in GATA4 phosphorylation and coincident reduction in GATA4-dependent transcriptional activity.
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