ArticleMolecular and cellular biology2010
Myocardin-related transcription factor A is a common mediator of mechanical stress- and neurohumoral stimulation-induced cardiac hypertrophic signaling leading to activation of brain natriuretic peptide gene expression.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 90 citations in OpenAlex.
- From gene to mechanics: a comprehensive insight into the mechanobiology of LMNA mutations in cardiomyopathy.Cell communication and signaling : CCS · 2024Review
- Exploring TTN variants as genetic insights into cardiomyopathy pathogenesis and potential emerging clues to molecular mechanisms in cardiomyopathies.Scientific reports · 2024Review
- Activation of an actin signaling pathway in pre-malignant mammary epithelial cells by P-cadherin is essential for transformation.Disease models & mechanisms · 2023Article
- NRSF/REST-Mediated Epigenomic Regulation in the Heart: Transcriptional Control of Natriuretic Peptides and Beyond.Biology · 2022Review
- Sensing and Responding of Cardiomyocytes to Changes of Tissue Stiffness in the Diseased Heart.Frontiers in cell and developmental biology · 2021Review
- Toward a New Paradigm for Targeted Natriuretic Peptide Enhancement in Heart Failure.Frontiers in physiology · 2021Review
- Myeloid MKL1 Disseminates Cues to Promote Cardiac Hypertrophy in Mice.Frontiers in cell and developmental biology · 2021Article
- Actin R256 Mono-methylation Is a Conserved Post-translational Modification Involved in Transcription.Cell reports · 2020Article
- Cancer associated fibroblast: Mediators of tumorigenesis.Matrix biology : journal of the International Society for Matrix Biology · 2020Review
- Mix and (mis-)match - The mechanosensing machinery in the changing environment of the developing, healthy adult and diseased heart.Biochimica et biophysica acta. Molecular cell research · 2020Review
- An MRTF-A-Sp1-PDE5 Axis Mediates Angiotensin-II-Induced Cardiomyocyte Hypertrophy.Frontiers in cell and developmental biology · 2020Article
- MRTF-A promotes angiotensin II-induced inflammatory response and aortic dissection in mice.PloS one · 2020Article
- Nucleoskeletal regulation of transcription: Actin on MRTF.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- The never-ending story of cardiac biomarkers: A further step toward a very early detection of ischemic patients?Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2019Article
- miR-486 is modulated by stretch and increases ventricular growth.JCI insight · 2019Article
- Article
- Translational science: Newly emerging science in biology and medicine - Lessons from translational research on the natriuretic peptide family and leptin.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2019Review
- Mechanosensitive Gene Regulation by Myocardin-Related Transcription Factors Is Required for Cardiomyocyte Integrity in Load-Induced Ventricular Hypertrophy.Circulation · 2018Article
- The Soft- and Hard-Heartedness of Cardiac Fibroblasts: Mechanotransduction Signaling Pathways in Fibrosis of the Heart.Journal of clinical medicine · 2017Review
- MKL1 defines the H3K4Me3 landscape for NF-κB dependent inflammatory response.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subjecting cardiomyocytes to mechanical stress or neurohumoral stimulation causes cardiac hypertrophy characterized in part by reactivation of the fetal cardiac gene program. Here we demonstrate a new common mechanism by which these stimuli are transduced to a signal activating the hypertrophic gene program. Mechanically stretching cardiomyocytes induced nuclear accumulation of myocardin-related transcription factor A (MRTF-A), a coactivator of serum response factor (SRF), in a Rho- and actin dynamics-dependent manner. Expression of brain natriuretic peptide (BNP) and other SRF-dependent fetal cardiac genes in response to acute mechanical stress was blunted in mice lacking MRTF-A. Hypertrophic responses to chronic pressure overload were also significantly attenuated in mice lacking MRTF-A. Mutation of a newly identified, conserved and functional SRF-binding site within the BNP promoter, or knockdown of MRTF-A, reduced the responsiveness of the BNP promoter to mechanical stretch. Nuclear translocation of MRTF-A was also involved in endothelin-1- and angiotensin-II-induced activation of the BNP promoter. Moreover, mice lacking MRTF-A showed significantly weaker hypertrophic responses to chronic angiotensin II infusion than wild-type mice. Collectively, these findings point to nuclear translocation of MRTF-A as a novel signaling mechanism mediating both mechanical stretch- and neurohumoral stimulation-induced BNP gene expression and hypertrophic responses in cardiac myocytes.
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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.