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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Background
TNF-α enhances contraction and inhibits endothelial NO-cGMP relaxation in systemic vessels of pregnant rats
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Background
Active Stabilization of Human Endothelial Nitric Oxide Synthase mRNA by hnRNP E1 Protects against Antisense RNA and MicroRNAs
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Background
Effect of clopidogrel on the expression of inflammatory markers in rabbit ischemic coronary artery
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Background
Priming of polymorphonuclear leukocytes: a culprit in the initiation of endothelial cell injury
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Background
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Background
Pro-inflammatory cytokines and endothelium-dependent vasodilation in the forearm. Serial assessment in patients with congestive heart failure
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Method
Nitric oxide synthase (NOS3) and contractile responsiveness to adrenergic and cholinergic agonists in the heart. Regulation of NOS3 transcription in vitro and in vivo by cyclic adenosine monophosphate in rat cardiac myocytes.
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Background
Striking crosstalk of ROCK signaling with endothelial function
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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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