ArticleJournal of lipid research2014
Determination of major UDP-glucuronosyltransferase enzymes and their genotypes responsible for 20-HETE glucuronidation.
Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Pharmacogenetics of Mycophenolic Acid in Patients of African Descent: Underrepresentation of African Data.Clinical and translational science · 2026Review
- Diclofenac-induced adverse drug reactions and hyperbilirubinemia caused by a variant gene.The Kaohsiung journal of medical sciences · 2022Article
- Drug-drug-gene interactions as mediators of adverse drug reactions to diclofenac and statins: a case report and literature review.Arhiv za higijenu rada i toksikologiju · 2021Review
- A Gilbert syndrome-associated haplotype protects against fatty liver disease in humanized transgenic mice.Scientific reports · 2020Article
- Conflicting roles of 20-HETE in hypertension and renal end organ damage.European journal of pharmacology · 2018Review
- Alterations in the gene expression of drug and arachidonic acid-metabolizing Cyp450 in the livers of controlled and uncontrolled insulin-dependent diabetic mice.Diabetes, metabolic syndrome and obesity : targets and therapy · 2018Article
- Effect of Cytochrome P450 Metabolites of Arachidonic Acid in Nephrology.Journal of the American Society of Nephrology : JASN · 2017Review
- Molecular mechanisms and cell signaling of 20-hydroxyeicosatetraenoic acid in vascular pathophysiology.Frontiers in bioscience (Landmark edition) · 2016Review
- Cytochrome P450 eicosanoids in hypertension and renal disease.Current opinion in nephrology and hypertension · 2015Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The compound 20-HETE is involved in numerous physiological functions, including blood pressure and platelet aggregation. Glucuronidation of 20-HETE by UDP-glucuronosyltransferases (UGTs) is thought to be a primary pathway of 20-HETE elimination in humans. The present study identified major UGT enzymes responsible for 20-HETE glucuronidation and investigated their genetic influence on the glucuronidation reaction using human livers (n = 44). Twelve recombinant UGTs were screened to identify major contributors to 20-HETE glucuronidation. Based on these results, UGT2B7, UGT1A9, and UGT1A3 exhibited as major contributors to 20-HETE glucuronidation. The Km values of 20-HETE glucuronidation by UGT1A3, UGT1A9, and UGT2B7 were 78.4, 22.2, and 14.8 μM, respectively, while Vmax values were 1.33, 1.78, and 1.62 nmol/min/mg protein, respectively. Protein expression levels and genetic variants of UGT1A3, UGT1A9, and UGT2B7 were analyzed in human livers using Western blotting and genotyping, respectively. Glucuronidation of 20-HETE was significantly correlated with the protein levels of UGT2B7 (r(2) = 0.33, P < 0.001) and UGT1A9 (r(2) = 0.31, P < 0.001), but not UGT1A3 (r(2) = 0.02, P > 0.05). A correlation between genotype and 20-HETE glucuronidation revealed that UGT2B7 802C>T, UGT1A9 -118T9>T10, and UGT1A9 1399T>C significantly altered 20-HETE glucuronide formation (P < 0.05-0.001). Increased levels of 20-HETE comprise a risk factor for cardiovascular diseases, and the present data may increase our understanding of 20-HETE metabolism and cardiovascular complications.
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