ArticleProceedings of the National Academy of Sciences of the United States of America2007
Angiotensin II up-regulates soluble epoxide hydrolase in vascular endothelium in vitro and in vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
85 citing papers in PubMed, 160 citations in OpenAlex.
- Fenofibrate lowers blood pressure in salt-sensitive but not salt-resistant hypertension.Journal of hypertension · 2013Trial
- Endothelium-derived hyperpolarizing factor determines resting and stimulated forearm vasodilator tone in health and in disease.Circulation · 2011Trial
- Trial
- General View of Arachidonic Acid (AA) Metabolism.Reviews of physiology, biochemistry and pharmacology · 2027Review
- Dual therapy with vildagliptin and sacubitril/valsartan alleviates portal hypertension and inhibits soluble epoxide hydrolase in cirrhotic rats.World journal of gastroenterology · 2025Article
- Overexpression of soluble epoxide hydrolase reduces post-ischemic recovery of cardiac contractile function.Biochemical pharmacology · 2024Article
- Tissue-, Region-, and Gene-Specific Induction of Microsomal Epoxide Hydrolase Expression and Activity in the Mouse Intestine by Arsenic in Drinking Water.Drug metabolism and disposition: the biological fate of chemicals · 2024Article
- Role of the soluble epoxide hydrolase in keratinocyte proliferation and sensitivity of skin to inflammatory stimuli.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
- The involvement of soluble epoxide hydrolase in the development of cardiovascular diseases through epoxyeicosatrienoic acids.Frontiers in pharmacology · 2024Review
- Increased Soluble Epoxide Hydrolase Activity Positively Correlates with Mortality in Heart Failure Patients with Preserved Ejection Fraction: Evidence from Metabolomics.Phenomics (Cham, Switzerland) · 2023Article
- Targeting IRE1α-JNK-c-Jun/AP-1-sEH Signaling Pathway Improves Myocardial and Coronary Endothelial Function Following Global Myocardial Ischemia/Reperfusion.International journal of medical sciences · 2022Article
- sEH promotes macrophage phagocytosis and lung clearance of Streptococcus pneumoniae.The Journal of clinical investigation · 2021Article
- Inhibition of Soluble Epoxide Hydrolase Attenuates Bosutinib-Induced Blood Pressure Elevation.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Activity of sEH and Oxidant Status during Systemic Bovine Coliform Mastitis.Antioxidants (Basel, Switzerland) · 2021Article
- Adenosine AMolecular and cellular biochemistry · 2021Article
- Treatment of Primary Aldosteronism Increases Plasma Epoxyeicosatrienoic Acids.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Discovery of Soluble Epoxide Hydrolase Inhibitors from Chemical Synthesis and Natural Products.Journal of medicinal chemistry · 2021Review
- The Role of Epoxyeicosatrienoic Acids in Cardiac Remodeling.Frontiers in physiology · 2021Review
- Inactivation of CysBritish journal of pharmacology · 2020Article
- The contribution of chymase-dependent formation of ANG II to cardiac dysfunction in metabolic syndrome of young rats: roles of fructose and EETs.American journal of physiology. Heart and circulatory physiology · 2020Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Epoxyeicosatrienoic acids (EETs), as metabolites of arachidonic acid, may function as antihypertensive and antiatherosclerotic mediators for vasculature. EETs are degraded by soluble epoxide hydrolase (sEH). Pharmacological inhibition and genetic ablation of sEH have been shown to increase the level of EETs, and treating angiotensin II (Ang II)-infused hypertension rats with sEH-selective inhibitors increased the levels of EETs, with attendant decrease in systolic blood pressure. To elucidate the mechanisms by which Ang II regulates sEH expression, we treated human umbilical vein endothelial cells (ECs) and bovine aortic ECs with Ang II and found increased sEH expression at both the mRNA and protein levels. Transient transfection assays showed that the activity of the human sEH promoter was increased in ECs in response to Ang II. Further analysis of the promoter region of the sEH gene demonstrated that treatment with Ang II, like overexpression of c-Jun/c-Fos, activates the sEH promoter through an AP-1-binding motif. The binding of c-Jun to the AP-1 site of the sEH promoter was confirmed by chromatin immunoprecipitation assays. In contrast, adenovirus overexpression of the dominant-negative mutant of c-Jun significantly attenuated the effects of Ang II on sEH induction. An elevated level of sEH was found in the aortic intima of both spontaneously hypertensive rats and Ang II-infused Wistar rats. Blocking Ang II binding to Ang II receptor 1 by losartan abolished the sEH induction. Thus, AP-1 activation is involved in the transcriptional up-regulation of sEH by Ang II in ECs, which may contribute to Ang II-induced hypertension.
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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.