ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2014
M3 mAChR-mediated IL-8 expression through PKC/NF-κB signaling pathways.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 7 citations in OpenAlex.
- Chronic stress drives gastric cancer lymph node metastasis via NETosis through a feedforward ACh-NGF axis-mediated PKC-γ/STAT3 pathway.Oncogene · 2026Article
- Cholinergic System and Its Therapeutic Importance in Inflammation and Autoimmunity.Frontiers in immunology · 2021Review
- New insights into mammalian signaling pathways using microfluidic pulsatile inputs and mathematical modeling.Integrative biology : quantitative biosciences from nano to macro · 2017Review
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8 authors at 1 institution in 1 country.
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Abstract
objectiveM3 muscarinic acetylcholine receptor (mAChR) plays an important role in the regulation of cytokine production in inflammatory diseases. In this study, we explored the precise role of M3 mAChR under stimulation with agonist in IL-8 expression and of the signaling pathway involved in this process. MATERIALS AND
methodsRecombinant U2OS cells stably expressing M3 mAChR as a model system were stimulated by carbachol to evaluate the role of M3 mAChR in the expression of IL-8.
resultsActivation of M3 mAChR with carbachol increased both IL-8 mRNA and protein expression in a concentration-dependent manner. Elevated IL-8 expression was completely antagonized by atropine, 4-DAMP and tiotropium. M3 mAChR-mediated IL-8 expression was almost completely inhibited by the NF-κB inhibitor BAY11-7082 and, to a lesser extent, by U0126, SB203580, and SP600125, which are inhibitors for ERK1/2, p38, and JNK, respectively. Furthermore, M3 mAChR-mediated NF-κB activation and IL-8 expression were simultaneously attenuated by the PKC inhibitor calphostin C, whereas PMA, a PKC activator, mimicked the effects of carbachol, inducing IL-8 expression.
conclusionsOur findings offer insights into the specific and critical role of M3 mAChR in regulating inflammatory response and indicate M3 mAChR/PKC/NF-κB signaling axis driven by endogenous acetylcholine as a potential therapeutic targets for inflammatory diseases.
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