ArticleThe Journal of clinical investigation1999
Mechanical strain activates BNP gene transcription through a p38/NF-kappaB-dependent mechanism.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 217 citations in OpenAlex.
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- CCN2/CTGF-Driven Myocardial Fibrosis and NT-proBNP Synergy as Predictors of Mortality in Maintenance Hemodialysis.International journal of molecular sciences · 2025Article
- Glucagon-like peptide-1 receptor: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024 · on this mapReview
- Markers of imminent myocardial infarction.Nature cardiovascular research · 2024Article
- Inhibition of ERK/CREB signaling contributes to postoperative learning and memory dysfunction in neonatal rats.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Cannabinoid receptor agonist attenuates angiotensin II-induced enlargement and mitochondrial dysfunction in rat atrial cardiomyocytes.Frontiers in pharmacology · 2023Article
- Transcriptomics reveal stretched human pluripotent stem cell-derived cardiomyocytes as an advantageous hypertrophy model.Journal of molecular and cellular cardiology plus · 2022Article
- Mechanical regulation of chromatin and transcription.Nature reviews. Genetics · 2022Review
- NRSF/REST-Mediated Epigenomic Regulation in the Heart: Transcriptional Control of Natriuretic Peptides and Beyond.Biology · 2022Review
- Review
- 6-Gingerol protects against cardiac remodeling by inhibiting the p38 mitogen-activated protein kinase pathway.Acta pharmacologica Sinica · 2021Article
- Integrins in cardiac hypertrophy: lessons learned from culture systems.ESC heart failure · 2021Review
- The role of mechanotransduction in heart failure pathobiology-a concise review.Heart failure reviews · 2021Review
- Cardiac Biomarkers and Autoantibodies in Endurance Athletes: Potential Similarities with Arrhythmogenic Cardiomyopathy Pathogenic Mechanisms.International journal of molecular sciences · 2021Review
- Nanoparticle-Mediated Angiotensin-(1-9) Drug Delivery for the Treatment of Cardiac Hypertrophy.Pharmaceutics · 2021Article
- Application of B-Type Natriuretic Peptide in Neonatal Diseases.Frontiers in pediatrics · 2021Review
- Progressive stretch enhances growth and maturation of 3D stem-cell-derived myocardium.Theranostics · 2021Article
- A combined bioinformatics, experimental and clinical approach to identify novel cardiac-specific heart failure biomarkers: is Dickkopf-3 (DKK3) a possible candidate?European journal of heart failure · 2020Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Application of mechanical strain to neonatal rat ventricular myocytes in culture evokes changes in gene expression reminiscent of those that occur with hypertrophy in vivo, such as stimulation of brain natriuretic peptide (BNP) gene expression. Here, we show that a major component of strain-dependent BNP promoter activation results from stimulation of p38 mitogen-activated protein kinase (MAPK) in the cardiac myocyte. Strain increased p38 activity in a time-dependent fashion. The p38 inhibitor SB203580 led to a reduction of approximately 60% in strain-activated human BNP (hBNP) promoter activity. Cotransfection of wild-type p38 increased both basal and strain-dependent promoter activity, while cotransfection with MKK6AL, a dominant-negative inhibitor of p38 MAPK kinase, resulted in partial inhibition of either p38- or strain-activated hBNP promoter activity. p38 MAPK increased hBNP promoter activity through activation of the transcription factor NF-kappaB. Activation of the hBNP promoter by either p38 or strain was mediated by DNA elements present in the 5' flanking sequence of the gene. Mechanical strain promoted assembly of NF-kappaB components on these DNA elements in vitro. Thus, induction of the hBNP promoter by mechanical strain depends, at least in part, on stimulation of p38 and subsequent activation of NF-kappaB. This activation may play an important role in signaling the increased BNP gene expression that accompanies hemodynamic overload and cardiac hypertrophy in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.