ArticlePediatric nephrology (Berlin, Germany)2006
Nitric oxide and superoxide in rat mesangial cells: modulation by C-reactive protein.
Article in Pediatric nephrology (Berlin, Germany), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Glomerular injury after trauma, burn, and sepsis.Journal of nephrology · 2023Review
- Asymmetric dimethylarginine and angiopoietin-like protein-2 are independent predictors of cardiovascular risk in pre-dialysis non-diabetic chronic kidney disease patients.International urology and nephrology · 2020Article
- The relation of C--reactive protein to chronic kidney disease in African Americans: the Jackson Heart Study.BMC nephrology · 2010Article
- C-reactive protein stimulates superoxide anion release and tissue factor activity in vivo.Atherosclerosis · 2009Article
- The evolving role of C-reactive protein in atherothrombosis.Clinical chemistry · 2009Review
- Human C-reactive protein accentuates macrophage activity in biobreeding diabetic rats.Journal of diabetes and its complicationsArticle
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundC-reactive protein (CRP) has been linked to cardiovascular and renal disease. We evaluated the effects of CRP on the production of nitric oxide (NO) and superoxide by rat mesangial cells (RMC) and the impact on cell function. METHODS AND
resultsRMC were incubated with cytokines (IFN-gamma, IL-1beta, and LPS) and CRP (10-100 microg/ml) for 24-72 h. Exposure to CRP resulted in a time- and dose-dependent reduction in NO accumulation (p<0.05). Although inducible nitric oxide synthase (iNOS) protein expression was unaltered after 48 h, CRP stimulated expression of HSP90. Steady state abundance of iNOS mRNA increased nearly threefold after a 24-h exposure to CRP. Incubation with 100 microg/ml CRP for 60-120 min resulted in a 272% increase in superoxide production that was prevented by diphenyleneiodium chloride but not L-NAME (p<0.0001).
conclusionCRP enhances superoxide release in RMC, which in turn inactivates NO and reduces net production. The functional relevance of these CRP-induced changes is supported by increased expression of HSP90 in RMC exposed to the mediator. These findings suggest that systemic inflammation, which contributes to the pathogenesis of atherosclerosis, may play a role in the progression of kidney disease.
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Registered trials
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.