ArticleProceedings of the National Academy of Sciences of the United States of America1998
Inhibition of hypoxia-inducible factor 1 activity by nitric oxide donors in hypoxia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
41 citing papers in PubMed, 228 citations in OpenAlex.
- NADPH Oxidase 4: Crucial for Endothelial Function under Hypoxia-Complementing Prostacyclin.Antioxidants (Basel, Switzerland) · 2024Article
- The adaptive strategies of yaks to live in the Asian highlands.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2022Review
- Chronic and Cycling Hypoxia: Drivers of Cancer Chronic Inflammation through HIF-1 and NF-κB Activation: A Review of the Molecular Mechanisms.International journal of molecular sciences · 2021Review
- Stemness of Human Pluripotent Cells: Hypoxia-Like Response Induced by Low Nitric Oxide.Antioxidants (Basel, Switzerland) · 2021Article
- Nitric oxide-releasing micelles with intelligent targeting for enhanced anti-tumor effect of cisplatin in hypoxia.Journal of nanobiotechnology · 2021Article
- Reduced Retinal Degeneration in an Oxidative Stress Organ Culture Model through an iNOS-Inhibitor.Biology · 2021Article
- HIF-1α Metabolic Pathways in Human Cancer.Advances in experimental medicine and biology · 2021Review
- Nitric Oxide Nano-Delivery Systems for Cancer Therapeutics: Advances and Challenges.Antioxidants (Basel, Switzerland) · 2020Review
- Inhibition of hypoxia-inducible factor 1α accumulation by glyceryl trinitrate and cyclic guanosine monophosphate.Bioscience reports · 2020Article
- Adaptation of Human iPSC-Derived Cardiomyocytes to Tyrosine Kinase Inhibitors Reduces Acute Cardiotoxicity via Metabolic Reprogramming.Cell systems · 2019Article
- PI3K/Akt signaling transduction pathway, erythropoiesis and glycolysis in hypoxia (Review).Molecular medicine reports · 2019Review
- The metal-nonoate Ni(SalPipNONO) inhibitsOncotarget · 2018Article
- Hypoxia-Inducible PIM Kinase Expression Promotes Resistance to Antiangiogenic Agents.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Hypoxia-Inducible Factor Stabilizers: a New Avenue for Reducing BP While Helping Hemoglobin?Current hypertension reports · 2016Review
- Nitric oxide from brain microvascular endothelial cells may initiate the compensatory response to mild hypoxia of astrocytes in a hypoxia-inducible factor-1α dependent manner.American journal of translational research · 2016Article
- Nitric oxide for cancer therapy.Future science OA · 2015Review
- Role of nitric oxide in the maintenance of pluripotency and regulation of the hypoxia response in stem cells.World journal of stem cells · 2015Review
- Repurposing Drugs in Oncology (ReDO)-nitroglycerin as an anti-cancer agent.Ecancermedicalscience · 2015Article
- Pharmacologic increase in HIF1α enhances hematopoietic stem and progenitor homing and engraftment.Blood · 2014Article
- Overexpression of extracellular superoxide dismutase protects against brain injury induced by chronic hypoxia.PloS one · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 O2 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 IC50 values of 7.8, 211, and 490 microM, 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 (IC50 = 6.6 microM). Induction generated by the addition of cobalt ion (this treatment mimics hypoxia) was also inhibited by SNP (IC50 = 2.5 microM). Increased luciferase activity expressed by cotransfection of effector plasmids for HIF-1alpha or HIF-1alpha-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-1alpha to a DNA-binding form.
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