Cited by 174Peroxisome Proliferator-Activated ReceptorsNitric Oxide and Endothelin EffectsParaoxonase enzyme and polymorphisms

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Peroxisome Proliferator-Activated Receptor α Agonists Increase Nitric Oxide Synthase Expression in Vascular Endothelial Cells

Goya, Kayoko, Sumitani, Satoru, Xu, Xin, Kitamura, Tetsuhiro, Yamamoto, Hiroyasu, Kurebayashi, Shogo, Saito, Hiroshi, Kouhara, Haruhiko, Kasayama, Soji, Kawase, Ichiro·2004·Arteriosclerosis, Thrombosis, and Vascular Biology

DOI 10.1161/01.atv.0000118682.58708.78

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Abstract

Objective— There has been accumulating evidence demonstrating that activators for peroxisome proliferator-activated receptor α (PPARα) have antiinflammatory, antiatherogenic, and vasodilatory effects. We hypothesized that PPARα activators can modulate endothelial nitric oxide synthase (eNOS) expression and its activity in cultured vascular endothelial cells. Methods and Results— Bovine aortic endothelial cells were treated with the PPARα activator fenofibrate. The amount of eNOS activity and the expression of eNOS protein and its mRNA were determined. Our data show that treatment with fenofibrate for 48 hours resulted in an increase in eNOS activity. Fenofibrate failed to increase eNOS activity within 1 hour. Fenofibrate also increased eNOS protein as well as its mRNA levels. RU486, which has been shown to antagonize PPARα action, inhibited the fenofibrate-induced upregulation of eNOS protein expression. WY14643 and bezafibrate also increased eNOS protein levels, whereas rosiglitazone did not. Transient transfection experiments using human eNOS promoter construct showed that fenofibrate failed to enhance eNOS promoter activity. Actinomycin D studies demonstrated that the half-life of eNOS mRNA increased with fenofibrate treatment. Conclusions— PPARα activators upregulate eNOS expression, mainly through mechanisms of stabilizing eNOS mRNA. This is a new observation to explain one of the mechanisms of PPARα-mediated cardiovascular protection.

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Authors: Goya, K., Sumitani, S., Xu, X., Kitamura, T., Yamamoto, H., Kurebayashi, S., Saito, H., Kouhara, H., Kasayama, S., & Kawase, I.
Affiliations: The University of Osaka (JP)
ORCID: Xu, Xin
Kitamura, Tetsuhiro
Yamamoto, Hiroyasu
Saito, Hiroshi
Kasayama, Soji
Kawase, Ichiro
Venue: Arteriosclerosis, Thrombosis, and Vascular Biology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2004-04
Volume: 24
Issue: 4
Pages: 658-663
ISSN: 1079-5642 (ISSN-L)
1524-4636
DOI: 10.1161/01.atv.0000118682.58708.78
OpenAlex: W2110733021
Cited by: 174
References: 47
Citations by year: 2026: 1 · 2025: 4 · 2024: 4 · 2023: 6 · 2022: 4 · 2021: 5 · 2020: 6 · 2019: 9 · 2017: 1 · 2016: 7 · 2015: 4 · 2014: 7 · 2013: 13 · 2012: 16
FWCI: 5.56
Type: journal article
Language: en
Open access: closed
Locations: Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
Keywords: PPARα agonist, endothelial nitric oxide synthase, fenofibrate, bezafibrate, Wy-14,643, rosiglitazone, RU486, vascular endothelial cells, cardioprotection
MeSH terms: Rosiglitazone, Animals, Aorta, Bezafibrate, Cattle, Cells, Cultured, Dactinomycin, Endothelium, Vascular, Enzyme Induction, Half-Life, Nitric Oxide, Fenofibrate, Pyrimidines, RNA, Messenger, Transcription Factors, Transcription, Genetic, Transfection, Mifepristone, Gene Expression Regulation, Enzymologic, Receptors, Cytoplasmic and Nuclear, Nitric Oxide Synthase, Endothelial Cells, Thiazolidinediones, Nitric Oxide Synthase Type III

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Peroxisome Proliferator-Activated Receptor α Agonists Increase Nitric Oxide Synthase Expression in Vascular Endothelial Cells

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