ArticleScientific reports2017
Hypertension reduces soluble guanylyl cyclase expression in the mouse aorta via the Notch signaling pathway.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Using an atlas of gene regulation across 44 human tissues to inform complex disease- and trait-associated variation.Nature genetics · 2018Pooled it
- MicroRNA-155 at the crossroads of inflammation and vascular dysfunction in essential hypertension.Molecular biology reports · 2026Review
- DAPT Mitigates Osteoarthritic Cartilage Degeneration and Enhances Articular Repair Through Targeted Modulation of the Gucy1a3 and Notch Signaling Axis.Drug design, development and therapy · 2026Article
- Soluble guanylate cyclase stimulators and activators as potential antihypertensive drugs.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Review
- Stimulating Soluble Guanylyl Cyclase with the Clinical Agonist Riociguat Restrains the Development and Progression of Castration-Resistant Prostate Cancer.Cancer research · 2025Article
- Promising Cerebral Blood Flow Enhancers in Acute Ischemic Stroke.Translational stroke research · 2023Review
- Genetics and mechanisms of thoracic aortic disease.Nature reviews. Cardiology · 2023Review
- Angiotensin II augments renal vascular smooth muscle soluble GC expression via an ATBritish journal of pharmacology · 2022Article
- Nitric Oxide Production and Regulation in the Teleost Cardiovascular System.Antioxidants (Basel, Switzerland) · 2022Review
- Sepsis downregulates aortic Notch signaling to produce vascular hyporeactivity in mice.Scientific reports · 2022Article
- Ligand-Independent G Protein-Coupled Estrogen Receptor/G Protein-Coupled Receptor 30 Activity: Lack of Receptor-Dependent Effects of G-1 and 17Molecular pharmacology · 2021Article
- Shared genetic architecture between neuroticism, coronary artery disease and cardiovascular risk factors.Translational psychiatry · 2021Article
- Editing of the myosin phosphatase regulatory subunit suppresses angiotensin II induced hypertension via sensitization to nitric oxide mediated vasodilation.Pflugers Archiv : European journal of physiology · 2021Article
- sGC Activity and Regulation of Blood Flow in a Zebrafish Model System.Frontiers in physiology · 2021Article
- Regulation of the Muscarinic MFrontiers in physiology · 2021Article
- Neurocardiac regulation: from cardiac mechanisms to novel therapeutic approaches.The Journal of physiology · 2020Review
- Pressurized carbon dioxide as a potential tool for decellularization of pulmonary arteries for transplant purposes.Scientific reports · 2020Article
- Reaching the End-Game for GWAS: Machine Learning Approaches for the Prioritization of Complex Disease Loci.Frontiers in genetics · 2020Review
- In utero exposure to maternal diabetes impairs nephron progenitor differentiation.American journal of physiology. Renal physiology · 2019Article
- Soluble guanylate cyclase contribute genetic susceptibility to essential hypertension in the Han Chinese population.Annals of translational medicine · 2019Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertension is a dominating risk factor for cardiovascular disease. To characterize the genomic response to hypertension, we administered vehicle or angiotensin II to mice and performed gene expression analyses. AngII treatment resulted in a robust increase in blood pressure and altered expression of 235 genes in the aorta, including Gucy1a3 and Gucy1b3 which encode subunits of soluble guanylyl cyclase (sGC). Western blotting and immunohistochemistry confirmed repression of sGC associated with curtailed relaxation via sGC activation. Analysis of transcription factor binding motifs in promoters of differentially expressed genes identified enrichment of motifs for RBPJ, a component of the Notch signaling pathway, and the Notch coactivators FRYL and MAML2 were reduced. Gain and loss of function experiments demonstrated that JAG/NOTCH signaling controls sGC expression together with MAML2 and FRYL. Reduced expression of sGC, correlating with differential expression of MAML2, in stroke prone and spontaneously hypertensive rats was also seen, and RNA-Seq data demonstrated correlations between JAG1, NOTCH3, MAML2 and FRYL and the sGC subunits GUCY1A3 and GUCY1B3 in human coronary artery. Notch signaling thus provides a constitutive drive on expression of the major nitric oxide receptor (GUCY1A3/GUCY1B3) in arteries from mice, rats, and humans, and this control mechanism is disturbed in hypertension.
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