Involvement of constitutive nitric oxide synthase in ghrelin-induced cytosolic phospholipase A2 activation in gastric mucosal cell protection against ethanol cytotoxicity

@article{Slomiany2009InvolvementOC,
  title={Involvement of constitutive nitric oxide synthase in ghrelin-induced cytosolic phospholipase A2 activation in gastric mucosal cell protection against ethanol cytotoxicity},
  author={B. L. Slomiany and Amalia Slomiany},
  journal={Inflammopharmacology},
  year={2009},
  volume={17},
  pages={245-253}
}
Ghrelin, an endogenous ligand for the growth hormone secretagogue receptor, is an important regulator of nitric oxide synthase (NOS) and cyclooxygenase (COX) enzyme systems, the products of which are of major significance to the processes of gastric mucosal defense and repair. Here, using primary culture of rat gastric mucosal cells, we report on the mechanism of ghrelin protection against ethanol cytotoxicity. We show that the protective effect of ghrelin was associated with the increase in NO… 
Cytosolic phospholipase A2 S-nitrosylation in ghrelin protection against detrimental effect of ethanol cytotoxicity on gastric mucin synthesis ——Ghrelin in gastric mucosal protection
TLDR
It is suggested that the activation of gastric mucosal cPLA2 through cNOS-induced S-nitrosylation plays an essential role in the countering effect of ghrelin on the disturbances in Gastric mucin synthesis caused by ethanol cytotoxicity.
Role of constitutive nitric oxide synthase in regulation of Helicobacter pylori-induced gastric mucosal cyclooxygenase-2 ac-tivation through S-nitrosylation: mechanism of ghrelin action
TLDR
It is demonstrated that induction in iNOS with H. pylori in- fection leads to COX-2 activation through S-nitro- sylation and up- regulation in PGE2 generation, and that ghrelin counters these untoward consequences of the LPS through Akt-mediated up-regulation in cNO- S activation required for the iN OS gene repression.
Cytosolic Phospholipase A2 S-Nitrosylation in Ghrelin Protection against Detrimental Effect of Ethanol Cytotoxicity on Gastric Mucin Synthesis
TLDR
It is suggested that the activation of gastric mucosal cPLA2 through cNOS-induced S-nitrosylation plays an essential role in the countering effect of ghrelin on the disturbances in Gastric mucin synthesis caused by ethanol cytotoxicity.
Ghrelin Protection against Lipopolysaccharide-Induced Gastric Mucosal Cell Apoptosis Involves Constitutive Nitric Oxide Synthase-Mediated Caspase-3 S-Nitrosylation
TLDR
Ghrelin protection of gastric mucosal cells against H. pylori LPS-induced apoptosis involves Src/Akt-mediated up-regulation in cNOS activation that leads to the apoptotic signal inhibition through the NO-induced caspase-3 S-nitrosylation.
Mechanism of Cytosolic Phospholipase A2 Activation in Ghrelin Protection of Salivary Gland Acinar Cells against Ethanol Cytotoxicity
TLDR
Ghrelin protection of salivary gland cells against ethanol involves cNOS-derived NO induction of cPLA2 activation through S-nitrosylation for the increase in AA release at the site of COX-1 action for PGE2 synthesis.
Role of constitutive nitric oxide synthase S-nitrosylation in Helicobacter pylori-induced gastric mucosal cell apoptosis: effect of ghrelin
TLDR
It is demonstrated that the disturbances in gastric mucosal NO generation system caused by H. pylori result from the iNOS-derived NO suppression of cNOS activation through S-nitrosylation.
Constitutive nitric oxide synthase-mediated caspase-3 S-nitrosylation in ghrelin protection against Porphyromonas gingivalis-induced salivary gland acinar cell apoptosis
TLDR
The findings point to the involvement of ghrelin in Src/Akt kinase-mediated cNOS activation and the apoptogenic signal inhibition through the NO-induced caspase-3 S-nitrosylation.
Induction in gastric mucosal prostaglandin and nitric oxide by Helicobacter pylori is dependent on MAPK/ERK-mediated activation of IKK-b and cPLA2: modulatory effect of ghrelin
TLDR
H. pylori-induced ERK activation plays a critical role in up-regulation of gastric mucosal PGE2 and NO generation at the level of IKK-b and cPLA2 activation, and that ghrelin counters these proinflammatory consequences of the LPS through Src/Akt-dependent S-nitrosylation.
Helicobacter pylori Induces Disturbances in Gastric Mucosal Akt Activation through Inducible Nitric Oxide Synthase-Dependent S-Nitrosylation: Effect of Ghrelin
TLDR
It is demonstrated that up-regulation in iNOS with H. pylori infection leads to Akt inactivation through S-nitrosylation that exerts the detrimental effect on the processes of cNOS activation through phosphorylation.
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
TLDR
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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References

SHOWING 1-10 OF 38 REFERENCES
Src kinase-mediated parallel activation of prostaglandin and constitutive nitric oxide synthase pathways in leptin protection of gastric mucosa against ethanol cytotoxicity.
  • B. Slomiany, A. Slomiany
  • Medicine, Biology
    Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
  • 2008
TLDR
It is demonstrated that leptin protection of gastric mucosa against ethanol cytotoxicity involves Src kinase-mediated bifurcated activation of MAPK/ERK and Akt that leads to up-regulation of the respective prostaglandin and nitric oxide synthase pathways.
Leptin-induced cytosolic phospholipase A2 activation in gastric mucosal protection against ethanol cytotoxicity involves epidermal growth factor receptor transactivation
TLDR
An important link between leptin-induced and Src kinase-mediated EGFR transactivation and the activation of cytosolic phospholipase A2 that leads to up-regulation in PGE2 production is disclosed, thus providing new insights into the mechanism of gastric mucosal protection by leptin.
Prostaglandin/Cyclooxygenase Pathway in Ghrelin-Induced Gastroprotection against Ischemia-Reperfusion Injury
TLDR
It is concluded that ghrelin exhibits gastroprotective and hyperemic activities against I/R-induced erosions, the effects that are mediated by hormone activation of GHS-R1a receptors, COX-PG system, and vagal-sensory nerves.
Modulation of Prostaglandin Biosynthesis by Nitric Oxide and Nitric Oxide Donors
TLDR
Experimental data is summarized that outline how the discovery that NO modulates prostaglandin production has impacted and extended the understanding of these two systems in physiopathological events.
Nitric Oxide Synthase/COX Cross-Talk: Nitric Oxide Activates COX-1 But Inhibits COX-2-Derived Prostaglandin Production1
TLDR
Divergent effects of NO on the COX isoforms are demonstrated, which indicate the regulation of PGE production by NO is therefore complex and will depend on the local environment in which these pleiotropic mediators are produced.
Regulation of Prostaglandin E2 Biosynthesis by Inducible Membrane-associated Prostaglandin E2 Synthase That Acts in Concert with Cyclooxygenase-2*
TLDR
COX-2 and mPGES are essential components for delayed PGE2 biosynthesis, which may be linked to inflammation, fever, osteogenesis, and even cancer.
Molecular mechanisms involved in the reciprocal regulation of cyclooxygenase and nitric oxide synthase enzymes.
TLDR
Experimental data is summarized that outline how the discovery that NO modulates PG production has impacted and extended the understanding of these two systems in physiopathological events.
Interference by leptin with Helicobacter pylori lipopolysaccharide-induced cytosolic phospholipase A2 activation in gastric mucosal cells.
  • B. Slomiany, A. Slomiany
  • Biology, Medicine
    Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
  • 2007
TLDR
It is shown that leptin counters the pathological consequences of H. pylori-induced cPLA(2) activation on gastric mucin synthesis through the involvement in signaling events controlled by MAPK/ERK and PI3K pathways.
Role of the different isoforms of cyclooxygenase and nitric oxide synthase during gastric ulcer healing in cyclooxygenase-1 and -2 knockout mice.
TLDR
It is demonstrated that COX-2 is a key mediator in gastric wound healing when COx-1 is unimpaired but becomes important when COX -2 is impaired, and that mRNA of COX and NOS isoforms were increased during healing inCOX-impaired mice.
...
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