ArticleThe Biochemical journal1996
Heat shock proteins and macrophage resistance to the toxic effects of nitric oxide.
Article in The Biochemical journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 74 citations in OpenAlex.
- The Influence of Oxidative Stress Markers in Patients with Ischemic Stroke.Biomolecules · 2024Review
- Emerging Targets for Modulation of Immune Response and Inflammation in Stroke.Neurochemical research · 2023Review
- Inhaled nitric oxide: role in the pathophysiology of cardio-cerebrovascular and respiratory diseases.Intensive care medicine experimental · 2022Review
- Heat shock protein 70B' (HSP70B') expression and release in response to human oxidized low density lipoprotein immune complexes in macrophages.The Journal of biological chemistry · 2010Article
- Molecular parameters of hyperthermia for radiosensitization.Critical reviews in eukaryotic gene expression · 2009Review
- Soy isoflavones reduce heat shock proteins in experimental atherosclerosis.European journal of nutrition · 2006Article
- Flow-mediated cell stress induction in adherent leukocytes is accompanied by modulation of morphology and phagocytic function.Medical & biological engineering & computing · 1999Article
- Macrophages resistant to endogenously generated nitric oxide-mediated apoptosis are hypersensitive to exogenously added nitric oxide donors: dichotomous apoptotic response independent of caspase 3 and reversal by the mitogen-activated protein kinase kinase (MEK) inhibitor PD 098059.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Inflammatory mediators are perpetuated in macrophages resistant to apoptosis induced by hypoxia.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Growth and viability of macrophages continuously stimulated to produce nitric oxide.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- The role of nitric oxide in stroke.Medical gas researchReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) functions as a pathophysiological mediator in mammalian tissues. Activated macrophages produce NO as a non-specific immune response directed against invading bacteria or micro-organisms. The same macrophages that initiate the production of NO also can be toxically affected by NO. Incubation of RAW 264.7 macrophages with lipopolysaccharide (LPS) and/or interferon-gamma (INF-gamma) induced the formation of NO by the activation of a cytokine-inducible NO synthase (NOS). The viability of these macrophages was inversely correlated with the formation of nitrite, a final NO-oxidation product measurable in the incubation medium. The addition of an NOS inhibitor, NG-monomethyl-L-arginine, diminished NO formation and preserved cell viability in a dose- and time-dependent fashion. Treatment of macrophages with ten cycles of non-lethal doses of LPS and INF-gamma, each followed by subculturing of the surviving cells, resulted in cell resistance to the NO toxic insult induced by LPS and INF-gamma. These resistant macrophages showed a 2-fold increase in the expression of the constitutive heat shock protein (HSC 70) which is known to be involved in protecting cells against the action of various metabolic insults. Our results establish a link between cell resistance to the toxic effects of NO, and the expression of heat shock proteins in RAW 264.7 macrophages.
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