ArticleThe Journal of surgical research2010
Cyclic AMP inhibits IL-1beta plus IFNgamma-induced NF-kappaB translocation in hepatocytes by a PKA independent mechanism.
Article in The Journal of surgical research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Elevated cAMP Protects against Diclofenac-Induced Toxicity in Primary Rat Hepatocytes: A Protective Effect Mediated by the Exchange Protein Directly Activated by cAMP/cAMP-Regulated Guanine Nucleotide Exchange Factors.Molecular pharmacology · 2021Article
- Neutrophils and the inflammatory tissue microenvironment in the mucosa.Immunological reviews · 2016Review
- Article
- Neutrophils and inflammatory resolution in the mucosa.Seminars in immunology · 2015Review
- Calcium-mediated signaling and calmodulin-dependent kinase regulate hepatocyte-inducible nitric oxide synthase expression.The Journal of surgical research · 2015Article
- Actions of adenosine on cullin neddylation: implications for inflammatory responses.Computational and structural biotechnology journal · 2015Review
- Activation of a cyclic amp-guanine exchange factor in hepatocytes decreases nitric oxide synthase expression.Shock (Augusta, Ga.) · 2013Article
- Insulin inhibits hepatocyte iNOS expression induced by cytokines by an Akt-dependent mechanism.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Cyclic AMP: a selective modulator of NF-κB action.Cellular and molecular life sciences : CMLS · 2011Review
- Article
- Akt-mediated signaling is induced by cytokines and cyclic adenosine monophosphate and suppresses hepatocyte inducible nitric oxide synthase expression independent of MAPK P44/42.Biochimica et biophysica acta · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We previously showed that cAMP inhibits IL-1beta plus IFNgamma-induced NF-kappaB binding in primary hepatocytes but the signaling mechanisms responsible for this effect are not understood. In this study, the role of PKA in mediating the effect of cAMP on NF-kappaB was investigated. Immunofluorescent staining showed that cAMP inhibited IL-1beta plus IFNgamma-induced translocation of NF-kappaB into the nucleus. Western blot analysis showed that the IL-1beta plus IFNgamma- induced phosphorylation and degradation of IkappaBa were markedly inhibited by cAMP. Immunocomplex assay involving GST-IKK revealed that cAMP inhibited IL-1beta plus IFNgamma-induced IKK activity. The PKA inhibitors had no effect on the inhibition of NF-kappaB binding by cAMP and did not change the p65 and IKB level induced by cAMP. Overexpression of PKA increased IL-1beta plus IFNgamma-induced NF-kappaB binding. These results suggest that PKA is not essential for the inhibitory effect of cAMP on NF-kappaB binding activity in hepatocytes. We demonstrated that cAMP inhibits IL-1beta plus IFNgamma-induced NF-kappaB binding due to its blockade of the upstream signal(s) leading to IkappaB phosphorylation and degradation, and is mediated by PKA-independent signaling pathways.
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Registered trials
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