ArticleThe Journal of clinical investigation1997
Nitric oxide induces heat-shock protein 70 expression in vascular smooth muscle cells via activation of heat shock factor 1.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 143 citations in OpenAlex.
- Regulatory interplay between nitric oxide and heme in redox signaling and inflammation.Redox biology · 2026Review
- Complete Immunophenotypic Reversal of Chronic Lymphocytic Leukaemia With High Dose Parenteral Methylcobalamin: A Case Report and Brief Review of Cobalamin in Cancer.Cancer reports (Hoboken, N.J.) · 2025Review
- β-Cell-selective regulation of gene expression by nitric oxide.American journal of physiology. Regulatory, integrative and comparative physiology · 2024Article
- Resolution of inflammation in chronic disease via restoration of the heat shock response (HSR).Cell stress & chaperones · 2024Review
- Proteotoxic stress response in atherosclerotic cardiovascular disease: Emerging role of heat shock factor 1.Frontiers in cardiovascular medicine · 2023Review
- Distinct patterns of responses in endothelial cells and smooth muscle cells following vascular injury.JCI insight · 2022Article
- Article
- Suppressed anti-inflammatory heat shock response in high-risk COVID-19 patients: lessons from basic research (inclusive bats), light on conceivable therapies.Clinical science (London, England : 1979) · 2020Review
- Regulation of stress signaling pathways by protein lipoxidation.Redox biology · 2019Review
- Nitric oxide metabolites in hypoxia, freezing, and hibernation of the wood frog, Rana sylvatica.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2018Article
- Heat shock protein 70/nitric oxide effect on stretched tubular epithelial cells linked to WT-1 cytoprotection during neonatal obstructive nephropathy.International urology and nephrology · 2017Article
- Mediators and mechanisms of heat shock protein 70 based cytoprotection in obstructive nephropathy.Cell stress & chaperones · 2015Review
- Arginine improves peroxisome functioning in cells from patients with a mild peroxisome biogenesis disorder.Orphanet journal of rare diseases · 2013Article
- Response of circulating heat shock protein 70 and anti-heat shock protein 70 antibodies to catheter ablation of atrial fibrillation.Journal of translational medicine · 2013Article
- Article
- Wt-1 Expression Linked to Nitric Oxide Availability during Neonatal Obstructive Nephropathy.Advances in urology · 2013Review
- Molecular mechanisms in exercise-induced cardioprotection.Cardiology research and practice · 2011Article
- Cardioprotective effects of nitrite during exercise.Cardiovascular research · 2011Review
- Neurotrophin-3 is a novel angiogenic factor capable of therapeutic neovascularization in a mouse model of limb ischemia.Arteriosclerosis, thrombosis, and vascular biology · 2010Article
- Expression of heat shock proteins and nitrotyrosine in small arteries from patients with coronary heart disease.Heart and vessels · 2009Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current data suggest that nitric oxide (NO) is a double-edged sword that could result in relaxation and/or cytotoxicity of vascular smooth muscle cells (SMCs) via cGMP- dependent or -independent signal pathways. Stress or heat shock proteins (hsps) have been shown to be augmented in arterial SMCs during acute hypertension and atherosclerosis, both conditions that are believed to correlate with disturbed NO production. In the present study, we demonstrate that NO generated from sodium nitroprusside (SNP), S-nitroso-N-acetylpenicillamine, and spermine/nitric oxide complex leads to hsp70 induction in cultured SMCs. Western blot analysis demonstrated that hsp70 protein expression peaked between 6 and 12 h after treatment with SNP, and elevated protein levels were preceded by induction of hsp70 mRNA within 3 h. Induction of hsp70 mRNA was associated with the activation of heat shock transcription factor 1 (HSF1), suggesting that the response was regulated at the transcriptional level. HSF1 activation was completely blocked by hemoglobin, dithiothreitol, and cycloheximide, suggesting that the protein damage and nascent polypeptide formation induced by NO may initiate this activation. Furthermore, SMCs pretreated with heat shock (42 degrees C) for 30 min were significantly protected from death induced by NO. Thus, we provide evidence that NO induces hsp70 expression in SMCs via HSF1 activation. Induction of hsp70 could be important in protecting SMCs from injury resulting from NO stimulation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.