ArticleMolecular and cellular biochemistry2013
C-reactive protein reduces protein S-nitrosylation in endothelial cells.
Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed, 6 citations in OpenAlex.
- NLRP3 inflammasome promotes diabetes-induced endothelial inflammation and atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019Article
- Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells.Endocrine · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C-reactive protein (CRP) emerges as an important mediator of cardiovascular lesions. In this study, we aimed to assess the role of CRP in the S-nitrosylation of proteins in endothelial cells and elucidate the potential mechanisms. Our results showed that CRP reduced protein S-nitrosylation in human umbilical vein endothelial cells (HUVECs). NO donor S-nitrosoglutathione antagonized CRP-mediated reduction of protein S-nitrosylation. Neutralizing antibody to Fcγ receptor II remarkably attenuated these changes. In addition, CRP increased NF-κB activation via the reduction of S-nitrosylation of p65, but not p50 in HUVECs, and induced the upregulation of NF-kB target gene vascular cell adhesion molecule-1. Furthermore, we confirmed that CRP reduced S-nitrosylated proteins in the rat aorta. Taken together, these data suggest that CRP-induced decline of protein S-nitrosylation by activating NF-κB via reduction of S-nitrosylation of p65, which may contribute to the endothelial dysfunction.
Indexed as
Identifiers
What OpenQuestion holds
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.