ArticleInflammation2016
Poly-L-Arginine Acts Synergistically with LPS to Promote the Release of IL-6 and IL-8 via p38/ERK Signaling Pathways in NCI-H292 Cells.
Article in Inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Poly-L-arginine promotes asthma angiogenesis through induction of FGFBP1 in airway epithelial cells via activation of the mTORC1-STAT3 pathway.Cell death & disease · 2021Article
- Amino Acids in Cell Signaling: Regulation and Function.Advances in experimental medicine and biology · 2021Article
- Pro-inflammatory effects of extracellular Hsp70 on NCI-H292 human bronchial epithelial cell line.International journal of experimental pathology · 2019Article
- Curcumin Attenuates Airway Inflammation and Airway Remolding by Inhibiting NF-κB Signaling and COX-2 in Cigarette Smoke-Induced COPD Mice.Inflammation · 2018Article
- Endothelial microparticles are increased in congenital heart diseases and contribute to endothelial dysfunction.Journal of translational medicine · 2017Article
- Article
- LPS Cooperates with Poly-L-Arginine to Promote IL-6 and IL-8 Release via the JNK Signaling Pathway in NCI-H292 Cells.Journal of immunology research · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Major basic protein (MBP) derived from activated eosinophil can exacerbate atopic asthma induced by lipopolysaccharide (LPS). The pharmacological function of MBP can be mimicked by poly-L-arginine (PLA), however, the potential signaling mechanisms of LPS-PLA-induced release of the inflammatory cytokines interleukin (IL)-6 and IL-8 remain unclear. In the present study, airway epithelia NCI-H292 cell lines were treated with LPS and/or PLA. We found that the expression levels of IL-6 and IL-8 induced by LPS-PLA were increased significantly compared with that in untreated cells. Meanwhile, the phosphorylation of p38 MAPK and ERK1/2 was also up-regulated dramatically by LPS-PLA, but this increase could be blocked by specific inhibitor. Importantly, blocking the phosphorylation of p38 MAPK and ERK1/2 reduced the expression levels of IL-6 and IL-8 as well. Collectively, LPS-PLA-induced release of IL-6 and IL-8 from NCI-H292 cells may be due to the synergistic activation of p38 MAPK and ERK1/2 signaling transduction pathways.
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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.