Cited by 224Cancer, Hypoxia, and MetabolismNitric Oxide and Endothelin EffectsErythropoietin and Anemia Treatment

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Inhibition of hypoxia-inducible factor 1 activity by nitric oxide donors in hypoxia

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Sogawa, Kazuhiro, Numayama-Tsuruta, Keiko, Ema, Masatsugu, Abe, Manabu, Abe, Hisaku, Fujii-Kuriyama, Yoshiaki·1998·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.95.13.7368PMC PMC22620

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Abstract

Nitric oxide (NO) is known to have various biologic and pathophysiologic effects on organisms. The molecular mechanisms by which NO exerts harmful effects are unknown, although various O 2 radicals and ions that result from reactivity of NO are presumed to be involved. Here we report that adaptive cellular response controlled by the transcription factor hypoxia-inducible factor 1 (HIF-1) in hypoxia is suppressed by NO. Induction of erythropoietin and glycolytic aldolase A mRNAs in hypoxically cultured Hep3B cells, a human hepatoma cell line, was completely and partially inhibited, respectively, by the addition of sodium nitroprusside (SNP), which spontaneously releases NO. A reporter plasmid carrying four hypoxia-response element sequences connected to the luciferase structural gene was constructed and transfected into Hep3B cells. Inducibly expressed luciferase activity in hypoxia was inhibited by the addition of SNP and two other structurally different NO donors, S -nitroso- l -glutathione and 3-morpholinosydnonimine, giving IC 50 values of 7.8, 211, and 490 μM, respectively. Inhibition by SNP was also observed in Neuro 2A and HeLa cells, indicating that the inhibition was not cell-type-specific. The vascular endothelial growth factor promoter activity that is controlled by HIF-1 was also inhibited by SNP (IC 50 = 6.6 μM). Induction generated by the addition of cobalt ion (this treatment mimics hypoxia) was also inhibited by SNP (IC 50 = 2.5 μM). Increased luciferase activity expressed by cotransfection of effector plasmids for HIF-1α or HIF-1α-like factor in hypoxia was also inhibited by the NO donor. We also showed that the inhibition was performed by blocking an activation step of HIF-1α to a DNA-binding form.

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Background
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Background
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Background
Endogenous nitric oxide attenuates erythropoietin gene expression in vivo
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Inhibition of hypoxia-inducible factor 1α accumulation by glyceryl trinitrate and cyclic guanosine monophosphate
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Stemness of Human Pluripotent Cells: Hypoxia-Like Response Induced by Low Nitric Oxide
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Authors: Sogawa, K., Numayama-Tsuruta, K., Ema, M., Abe, M., Abe, H., & Fujii-Kuriyama, Y.
Affiliations: Tohoku University (JP)
Department of Chemistry, Graduate School of Science, Tohoku University, Aoba-ku, Sendai 980-77, Japan
ORCID: Sogawa, Kazuhiro
Ema, Masatsugu
Abe, Manabu
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 1998-06-23
Volume: 95
Issue: 13
Pages: 7368-7373
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.95.13.7368
PMC: PMC22620
OpenAlex: W2046905314
Cited by: 224
References: 51
Citations by year: 2026: 1 · 2024: 2 · 2022: 3 · 2021: 11 · 2020: 3 · 2019: 3 · 2018: 3 · 2017: 3 · 2016: 3 · 2015: 8 · 2014: 8 · 2013: 8 · 2012: 3
FWCI: 4.06
Type: journal article
Language: en
Open access: green
europepmc.org
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
Keywords: HIF-1, nitric oxide donors, hypoxia, erythropoietin, aldolase A, vascular endothelial growth factor, hypoxia response element, sodium nitroprusside, SIN-1, transcriptional regulation
MeSH terms: Cells, Cultured, DNA, DNA-Binding Proteins, Enzyme Induction, Erythropoietin, Fructose-Bisphosphate Aldolase, Humans, Nitric Oxide, Nitroprusside, Nuclear Proteins, RNA, Messenger, Transcription Factors, Transcription, Genetic, Transfection, Cell Hypoxia, Helix-Loop-Helix Motifs, Hypoxia-Inducible Factor 1, Hypoxia-Inducible Factor 1, alpha Subunit

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Inhibition of hypoxia-inducible factor 1 activity by nitric oxide donors in hypoxia

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