ArticleArteriosclerosis, thrombosis, and vascular biology2012
Opposing actions of heat shock protein 90 and 70 regulate nicotinamide adenine dinucleotide phosphate oxidase stability and reactive oxygen species production.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 85 citations in OpenAlex.
- Exogenous Heat Shock Proteins in Oncology: Biological Roles and Clinical Implications.Cancers · 2026Review
- Bio fluid exosomes: promises, challenges, and future directions in translational medicine.Journal of translational medicine · 2025Review
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Immunoexpression Pattern of Autophagy-Related Proteins in Human Congenital Anomalies of the Kidney and Urinary Tract.International journal of molecular sciences · 2024Article
- Chaperones vs. oxidative stress in the pathobiology of ischemic stroke.Frontiers in molecular neuroscience · 2024Review
- Functional interactions between NADPH oxidase 5 and actin.Frontiers in cell and developmental biology · 2023Article
- EROS is a selective chaperone regulating the phagocyte NADPH oxidase and purinergic signalling.eLife · 2022Article
- Hif-1α/Hsf1/Hsp70 signaling pathway regulates redox homeostasis and apoptosis in large yellow croaker (Zoological research · 2021Article
- Suppression of reactive oxygen species in endothelial cells by an antagonist of growth hormone-releasing hormone.Journal of biochemical and molecular toxicology · 2021Article
- Nitric oxide and heme-NO stimulate superoxide production by NADPH oxidase 5.Free radical biology & medicine · 2021Article
- Overexpression of heat shock protein 70 inhibits epithelial-mesenchymal transition and cell migration induced by transforming growth factor-β in A549 cells.Cell stress & chaperones · 2021Article
- NADPH Oxidase 5 Induces Changes in the Unfolded Protein Response in Human Aortic Endothelial Cells and in Endothelial-SpecificAntioxidants (Basel, Switzerland) · 2021Article
- The Hsp90 Inhibitor 17-DMAG Attenuates Hyperglycemia-Enhanced Hemorrhagic Transformation in Experimental Stroke.BioMed research international · 2021Article
- Beyond the Extra Respiration of Phagocytosis: NADPH Oxidase 2 in Adaptive Immunity and Inflammation.Frontiers in immunology · 2021Review
- Heat shock increases hydrogen peroxide release from circulating hemocytes of the snail Biomphalaria glabrata.Fish & shellfish immunology · 2020Article
- Endothelial or vascular smooth muscle cell-specific expression of human NOX5 exacerbates renal inflammation, fibrosis and albuminuria in the Akita mouse.Diabetologia · 2019Article
- Quantitative proteomic analysis reveals AK2 as potential biomarker for late normal tissue radiotoxicity.Radiation oncology (London, England) · 2019Article
- Galectin-3 is expressed in vascular smooth muscle cells and promotes pulmonary hypertension through changes in proliferation, apoptosis, and fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- A coumarin analogue NFA from endophytic Aspergillus fumigatus improves drought resistance in rice as an antioxidant.BMC microbiology · 2019Article
- Immunogenic Effect of Hyperthermia on Enhancing Radiotherapeutic Efficacy.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
12 authors at 8 institutions in 4 countries.
Funding
Abstract
objectiveExcessive reactive oxygen species contribute to vascular dysfunction. We have previously shown that heat shock protein (Hsp90) inhibitors potently suppress Nox 1 to 3 and 5, and the goals of this study were to identify how molecular chaperones regulate Nox function. METHODS AND
resultsIn vitro, protein expression of Nox 1 to 2, 5 was decreased by Hsp90 inhibitors in multiple cell types (human pulmonary artery endothelial cells, neutrophils, macrophages, and human saphenous vein). In mice treated with Hsp90 inhibitors, Nox1 expression was reduced in lung along with reduced reactive oxygen species from leukocytes. Elevated reactive oxygen species production in obese (db/db) aorta was suppressed by Hsp90 inhibition. Hsp90 inhibitors did not alter Nox5 micro RNA levels, and proteasome inhibition prevented Nox2 and 5 protein degradation and increased ubiquitin incorporation. Inhibition of Hsp90 upregulated the expression of Hsp70 and Hsp70-bound Nox2, 5 and promoted degradation. Silencing Hsp70 prevented Hsp90 inhibitor-mediated degradation of Nox5. The Hsp70-regulated ubiquitin ligase, carboxyl terminus of Hsp70-interacting protein (CHIP), also bound Nox5 and promoted increased Nox5 ubiquitination and degradation. The chaperone binding and ubiquitination domains of CHIP were required, and the silencing of CHIP blunted Hsp90 inhibitor-mediated degradation of Nox2 and 5.
conclusionsWe conclude that Hsp90 binds to and regulates Nox protein stability. These actions are opposed by Hsp70 and CHIP, which promote the ubiquitination and degradation of Nox proteins and reduce reactive oxygen species production.
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