ArticleJournal of molecular and cellular cardiology2014
Orphan nuclear receptor Nur77 is a novel negative regulator of endothelin-1 expression in vascular endothelial cells.
Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Nuclear receptor Nur77 resolves the inflammatory response of macrophages primarily by regulating expression of AP-1 transcription factors and their target genes.Nucleic acids research · 2026Article
- Targeting Inflammation: Cytosporone B Modulates Imatinib-Driven Biochemical Alterations in Rat Heart.International journal of molecular sciences · 2025Article
- Critical roles of chronic BCR signaling in the differentiation of anergic B cells into age-associated B cells in aging and autoimmunity.Science advances · 2025Article
- HPGD: An Intermediate Player in Microglial Polarization and Multiple Sclerosis Regulated by Nr4a1.Molecular neurobiology · 2025Article
- Inhibiting endothelial cell Mst1 attenuates acute lung injury in mice.JCI insight · 2024Article
- Natural products and synthetic analogs as selective orphan nuclear receptor 4A (NR4A) modulators.Histology and histopathology · 2024Review
- Liquiritin exhibits anti-acute lung injury activities through suppressing the JNK/Nur77/c-Jun pathway.Chinese medicine · 2023Article
- NDRG1 Signaling Is Essential for Endothelial Inflammation and Vascular Remodeling.Circulation research · 2023Article
- Nur77 Deficiency Exacerbates Macrophage NLRP3 Inflammasome-Mediated Inflammation and Accelerates Atherosclerosis.Oxidative medicine and cellular longevity · 2022Article
- Emodin Protects Against Lipopolysaccharide-Induced Acute Lung InjuryFrontiers in pharmacology · 2022Article
- Nur77 Attenuates Inflammasome Activation by Inhibiting Caspase-1 Expression in Pulmonary Vascular Endothelial Cells.American journal of respiratory cell and molecular biology · 2021Article
- Untangling the Cooperative Role of Nuclear Receptors in Cardiovascular Physiology and Disease.International journal of molecular sciences · 2021Review
- From sepsis to acute respiratory distress syndrome (ARDS): emerging preventive strategies based on molecular and genetic researches.Bioscience reports · 2020Review
- Effects of coal-fired PMBMC pharmacology & toxicology · 2020Article
- Simvastatin Suppresses Human Breast Cancer Cell Invasion by Decreasing the Expression of Pituitary Tumor-Transforming Gene 1.Frontiers in pharmacology · 2020Article
- Nur77 limits endothelial barrier disruption to LPS in the mouse lung.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- The Mechanism of Acupuncture in Treating Essential Hypertension: A Narrative Review.International journal of hypertension · 2019Review
- Transcriptional up-regulation of relaxin-3 by Nur77 attenuates β-adrenergic agonist-induced apoptosis in cardiomyocytes.The Journal of biological chemistry · 2018Article
- Mechanotransduction in Coronary Vein Graft Disease.Frontiers in cardiovascular medicine · 2018Article
- Nuclear Receptor Nur77 Deficiency Alters Dendritic Cell Function.Frontiers in immunology · 2018Article
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Endothelin-1 (ET-1) produced by vascular endothelial cells plays essential roles in the regulation of vascular tone and development of cardiovascular diseases. The objective of this study is to identify novel regulators implicated in the regulation of ET-1 expression in vascular endothelial cells (ECs). By using quantitative real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA), we show that either ectopic expression of orphan nuclear receptor Nur77 or pharmacological activation of Nur77 by 6-mercaptopurine (6-MP) substantially inhibits ET-1 expression in human umbilical vein endothelial cells (HUVECs), under both basal and thrombin-stimulated conditions. Furthermore, thrombin-stimulated ET expression is significantly augmented in both Nur77 knockdown ECs and aort from Nur77 knockout mice, suggesting that Nur77 is a negative regulator of ET-1 expression. Inhibition of ET-1 expression by Nur77 occurs at gene transcriptional levels, since Nur77 potently inhibits ET-1 promoter activity, without affecting ET-1 mRNA stability. As shown in electrophoretic mobility shift assay (EMSA), Nur77 overexpression markedly inhibits both basal and thrombin-stimulated transcriptional activity of AP-1. Mechanistically, we demonstrate that Nur77 specially interacts with c-Jun and inhibits AP-1 dependent c-Jun promoter activity, which leads to a decreased expression of c-Jun, a critical component involved in both AP-1 transcriptional activity and ET-1 expression in ECs. These findings demonstrate that Nur77 is a novel negative regulator of ET-1 expression in vascular ECs through an inhibitory interaction with the c-Jun/AP-1 pathway. Activation of Nur77 may represent a useful therapeutic strategy for preventing certain cardiovascular diseases, such as atherosclerosis and pulmonary artery hypertension.
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