ArticleInflammopharmacology2013
Induction in gastric mucosal prostaglandin and nitric oxide by Helicobacter pylori is dependent on MAPK/ERK-mediated activation of IKK-β and cPLA2: modulatory effect of ghrelin.
Article in Inflammopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- A2BR facilitates the pathogenesis of H. pylori-associated GU by inducing oxidative stress through p38 MAPK phosphorylation.Heliyon · 2023Article
- Mechanisms of Dendrobium officinale polysaccharides in repairing gastric mucosal injuries based on mitogen-activated protein kinases (MAPK) signaling pathway.Bioengineered · 2022Article
- Impact ofMicroorganisms · 2021Review
- Relationship BetweenInternational journal of general medicine · 2021Review
- Anti-microbial and anti-inflammatory effects of Cheonwangbosim-dan againstJournal of veterinary science · 2020Article
- Syk: a new target for attenuation of Helicobacter pylori-induced gastric mucosal inflammatory responses.Inflammopharmacology · 2019Review
- Helicobacter pylori LPS-induced gastric mucosal spleen tyrosine kinase (Syk) recruitment to TLR4 and activation occurs with the involvement of protein kinase Cδ.Inflammopharmacology · 2018Article
- Observational
- Mechanisms of Antiulcer Effect of an Active Ingredient Group of Modified Xiao Chaihu Decoction.Evidence-based complementary and alternative medicine : eCAM · 2018Article
- Article
- Role of LPS-elicited signaling in triggering gastric mucosal inflammatory responses to H. pylori: modulatory effect of ghrelin.Inflammopharmacology · 2017Review
- Ghrelin and gastrointestinal stromal tumors.World journal of gastroenterology · 2017Review
- Helicobacter pylori-induced changes in microtubule dynamics conferred by α-tubulin phosphorylation on Ser/Tyr mediate gastric mucosal secretion of matrix metalloproteinase-9 (MMP-9) and its modulation by ghrelin.Inflammopharmacology · 2016Article
- Role of protein kinase D2 phosphorylation on Tyr in modulation by ghrelin of Helicobacter pylori-induced up-regulation in gastric mucosal matrix metalloproteinase-9 (MMP-9) secretion.Inflammopharmacology · 2016Article
- Helicobacter pylori-elicited induction in gastric mucosal matrix metalloproteinase-9 (MMP-9) release involves ERK-dependent cPLA2 activation and its recruitment to the membrane-localized Rac1/p38 complex.Inflammopharmacology · 2016Article
- Simvastatin and a Plant Galactolipid Protect Animals from Septic Shock by Regulating Oxylipin Mediator Dynamics through the MAPK-cPLAMolecular medicine (Cambridge, Mass.) · 2016Article
- Helicobacter pylori-induced gastric mucosal TGF-α ectodomain shedding and EGFR transactivation involves Rac1/p38 MAPK-dependent TACE activation.Inflammopharmacology · 2016Article
- Gypenoside Protects Cardiomyocytes against Ischemia-Reperfusion Injury via the Inhibition of Mitogen-Activated Protein Kinase Mediated Nuclear Factor Kappa B Pathway In Vitro and In Vivo.Frontiers in pharmacology · 2016Article
- From the stomach to other organs: Helicobacter pylori and the liver.World journal of hepatology · 2015Review
- Mechanism of Rac1-induced amplification in gastric mucosal phospholipase Cγ2 activation in response to Helicobacter pylori: modulatory effect of ghrelin.Inflammopharmacology · 2015Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Among the key factors defining the extent of gastric mucosal inflammatory involvement in response to Helicobacter pylori is the excessive generation of prostaglandin (PGE2) and nitric oxide (NO), caused by the overexpression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), and triggered by the activation of mitogen-activated protein kinase (MAPK)/c-Jun N-terminal kinase, p38 and ERK, and nuclear translocation of the cognate transcription factors. In this study, we report on the role of MAPK/ERK in the regulation of H. pylori LPS-induced gastric mucosal expression of COX-2 and iNOS. We show that ERK activation by the LPS leads to phosphorylation of the inhibitory κB kinase-β (IKK-β) and cytosolic phospholipase A2 (cPLA2), and is reflected in the upsurge in NF-κB nuclear translocation, induction in COX-2 and iNOS expression, and up-regulation in cPLA2 activity. The modulatory effect of peptide hormone, ghrelin, on the LPS-induced changes, although associated with further enhancement in ERK, IKK-β, and cPLA2 phosphorylation, was reflected in the suppression of IKK-β and cPLA2 activity through S-nitrosylation. While the effect of ghrelin on S-nitrosylation was susceptible to suppression by the inhibitors of Src/Akt pathway, the inhibition of ERK activation caused the blockage in IKK-β and cPLA2 phosphorylation as well as S-nitrosylation. Taken together, our data show that H. pylori-induced ERK activation plays a critical role in up-regulation of gastric mucosal PGE2 and NO generation at the level of IKK-β and cPLA2 activation, and that ghrelin counters these proinflammatory consequences of the LPS through Src/Akt-dependent S-nitrosylation.
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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.