ArticleScientific reports2017
MKP-1 negative regulates Staphylococcus aureus induced inflammatory responses in Raw264.7 cells: roles of PKA-MKP-1 pathway and enhanced by rolipram.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Protective effects of rolipram on endotoxic cardiac dysfunction via inhibition of the inflammatory response in cardiac fibroblasts.BMC cardiovascular disorders · 2020Article
- Pharmacological inhibition of MKP-1 exacerbates central post-stroke pain and neuroinflammation in mice.Molecular painArticle
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
MAP phosphatases (MKP)-1 acts as an important regulator of innate immune response through a mechanism of control and attention both MAPK and NF-κB molecules during bacterial infection. However, the regulatory role of MKP-1 in the interplay between MAPK and NFκB pathway molecules is still not fully understood. In present study, we showed a direct interactions of p38, ERK or IκBα with MKP-1, and demonstrated that MKP-1 was a pivotal feedback control for both MAP kinases and NF-κB pathway in response to S. aureus. In addition, we found that rolipram had anti-inflammatory activity and repressed IκBα activation induced by S. aureus via PKA-MKP-1 pathway. Our report also demonstrated that PKA-cα can directly bind to IκBα upon S. aureus stimulation, which influenced the downstream signaling of PKA pathway, including altered the expression of MKP-1. These results presented a novel mechanism of PKA and IκB pathway, which may be targeted for treating S. aureus infection.
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Registered trials
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