Cited by 775Nitric Oxide and Endothelin EffectsAtherosclerosis and Cardiovascular DiseasesAngiogenesis and VEGF in Cancer

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Tumor necrosis factor downregulates an endothelial nitric oxide synthase mRNA by shortening its half-life

Yoshizumi, M, Perrella, M A, Burnett, J C, Lee, M E·1993·Circulation Research

DOI 10.1161/01.res.73.1.205

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Abstract

Nitric oxide (NO), which accounts for the biological properties of endothelium-derived relaxing factor, is generated by NO synthase (NOS). The vascular endothelium contains two types of NOS: one is constitutively expressed (cNOS), and the other is inducible. Endothelium-mediated vasorelaxation is impaired in atherosclerotic vessels. To determine whether tumor necrosis factor (TNF)-alpha, which is commonly found in atherosclerotic lesions, has an effect on NOS message, we measured cNOS mRNA levels in TNF-treated human umbilical vein endothelial cells (HUVECs) by RNA blot analysis with a cNOS cDNA probe. TNF-alpha markedly reduced cNOS mRNA levels in HUVECs in a dose- and time-dependent manner. In response to 3 ng/mL TNF-alpha, cNOS mRNA levels began to decrease at 4 hours and diminished to only 5% of control levels at 24 hours. As little as 0.1 ng/mL TNF-alpha reduced cNOS mRNA levels by 50%. This reduction in cNOS message in response to TNF-alpha depended on protein synthesis as it was blocked by cycloheximide. In nuclear runoff experiments, TNF-alpha did not change the rate of cNOS gene transcription. cNOS mRNA is very stable under basal conditions, with a half-life of 48 hours; however, treatment with TNF-alpha shortened this half-life to 3 hours. TNF-alpha thus appears to decrease cNOS mRNA levels by increasing the rate of mRNA degradation. TNF-induced reductions in cNOS mRNA levels may have an important effect on impaired endothelium-mediated vasorelaxation in atherosclerosis.

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Authors: Yoshizumi, M., Perrella, M. A., Burnett, J. C., & Lee, M. E.
Affiliations: Harvard University (US)
ORCID: Yoshizumi, M
Perrella, M A
Venue: Circulation Research
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 1993-07
Volume: 73
Issue: 1
Pages: 205-209
ISSN: 0009-7330 (ISSN-L)
1524-4571
DOI: 10.1161/01.res.73.1.205
OpenAlex: W2145570729
Cited by: 771
References: 0
Citations by year: 2026: 4 · 2025: 5 · 2024: 9 · 2023: 10 · 2022: 13 · 2021: 15 · 2020: 16 · 2019: 12 · 2018: 16 · 2017: 14 · 2016: 11 · 2015: 17 · 2014: 35 · 2013: 19 · 2012: 18
FWCI: 21.77
Type: journal article
Language: en
Open access: closed
Locations: Circulation Research (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
Keywords: TNF-α, endothelial nitric oxide synthase, constitutive nitric oxide synthase, mRNA stability, mRNA degradation, human umbilical vein endothelial cells, atherosclerosis, cycloheximide, gene transcription
MeSH terms: Amino Acid Oxidoreductases, Base Sequence, Endothelium, Vascular, Half-Life, Humans, Molecular Sequence Data, RNA, Messenger, Transcription, Genetic, Tumor Necrosis Factor-alpha, Umbilical Veins, Down-Regulation, Polymerase Chain Reaction, Nitric Oxide Synthase

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Tumor necrosis factor downregulates an endothelial nitric oxide synthase mRNA by shortening its half-life

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