ArticleInternational journal of cardiology2013
A potent soluble epoxide hydrolase inhibitor, t-AUCB, acts through PPARγ to modulate the function of endothelial progenitor cells from patients with acute myocardial infarction.
Article in International journal of cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 62 citations in OpenAlex.
- The involvement of soluble epoxide hydrolase in the development of cardiovascular diseases through epoxyeicosatrienoic acids.Frontiers in pharmacology · 2024Review
- In Silico Modeling and Structural Analysis of Soluble Epoxide Hydrolase Inhibitors for Enhanced Therapeutic Design.Molecules (Basel, Switzerland) · 2023Article
- Dual soluble epoxide hydrolase inhibitor - farnesoid X receptor agonist interventional treatment attenuates renal inflammation and fibrosis.Frontiers in immunology · 2023Article
- Decreased Expression of Soluble Epoxide Hydrolase Suppresses Murine Choroidal Neovascularization.International journal of molecular sciences · 2022Article
- Endothelial progenitor cells and coronary artery disease: Current concepts and future research directions.World journal of clinical cases · 2021Review
- Metabolism pathways of arachidonic acids: mechanisms and potential therapeutic targets.Signal transduction and targeted therapy · 2021Review
- Discovery of Soluble Epoxide Hydrolase Inhibitors from Chemical Synthesis and Natural Products.Journal of medicinal chemistry · 2021Review
- Soluble Epoxide Hydrolase Inhibition byInternational journal of molecular sciences · 2020Article
- Exosomes from SIRT1-Overexpressing ADSCs Restore Cardiac Function by Improving Angiogenic Function of EPCs.Molecular therapy. Nucleic acids · 2020Article
- Soluble Epoxide Hydrolase Inhibition in Liver Diseases: A Review of Current Research and Knowledge Gaps.Biology · 2020Review
- A novel interaction between soluble epoxide hydrolase and the AT1 receptor in retinal microvascular damage.Prostaglandins & other lipid mediators · 2020Article
- Article
- Cytochrome P450 derived epoxidized fatty acids as a therapeutic tool against neuroinflammatory diseases.Prostaglandins & other lipid mediators · 2020Review
- Protostane-type triterpenoids as natural soluble epoxide hydrolase inhibitors: Inhibition potentials and molecular dynamics.Bioorganic chemistry · 2020Article
- Multi-Target Approaches in Metabolic Syndrome.Frontiers in pharmacology · 2020Review
- Comprehensive analysis of competing endogenous RNA networks associated with cholangiocarcinoma.Experimental and therapeutic medicine · 2019Article
- Inhibition of Pancreatic Carcinoma Growth Through Enhancing ω-3 Epoxy Polyunsaturated Fatty Acid Profile by Inhibition of Soluble Epoxide Hydrolase.Anticancer research · 2019Article
- Epoxyeicosatrienoic acid analog EET-B attenuates post-myocardial infarction remodeling in spontaneously hypertensive rats.Clinical science (London, England : 1979) · 2019Article
- Substrate and inhibitor selectivity, and biological activity of an epoxide hydrolase from Trichoderma reesei.Molecular biology reports · 2019Article
- Zafirlukast Is a Dual Modulator of Human Soluble Epoxide Hydrolase and Peroxisome Proliferator-Activated Receptor γ.Frontiers in pharmacology · 2019Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundEpoxyeicosatrienoic acids (EETs) are natural angiogenic mediators regulated by soluble epoxide hydrolase (sEH). Inhibitors of sEH can stabilize EETs levels and were reported to reduce atherosclerosis and inhibit myocardial infarction in animal models. In this work, we investigated whether increasing EETs with the sEH inhibitor t-AUCB would increase angiogenesis related function in endothelial progenitor cells (EPCs) from patients with acute myocardial infarction (AMI). METHODS AND
resultsEPCs were isolated from 50 AMI patients and 50 healthy subjects (control). EPCs were treated with different concentrations of t-AUCB for 24h with or without peroxisome proliferator activated receptor γ (PPARγ) inhibitor GW9662. Migration of EPCs was assayed in trans-well chambers. Angiogenesis assays were performed using a Matrigel-Matrix in vitro model. The expression of vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1α (HIF-1α) mRNA and protein in EPCs was measured by real-time PCR or Western blot, respectively. Also, the concentration of EETs in the culture supernatant was detected by ELISA. The activity of EPCs in the AMI patient group was reduced compared to healthy controls. Whereas increasing EET levels with t-AUCB promoted a dose dependent angiogenesis and migration in EPCs from AMI patients. Additionally, the t-AUCB dose dependently increased the expression of the angiogenic factors VEGF and HIF-α. Lastly, we provide evidence that these effects were PPARγ dependent.
conclusionThe results demonstrate that the sEH inhibitor positively modulated the functions of EPCs in patients with AMI through the EETs-PPARγ pathway. The present study suggests the potential utility of sEHi in the therapy of ischemic heart disease.
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