%0 Journal Article
%T Ghrelin Suppression of <i>Helicobacter pylori</i>-Induced Gastric Mucosal Expression of iNOS is Mediated through the Inhibition of IKK-<i>¦Â</i> Activation by cNOS-Dependent S-Nitrosylation
%A Bronislaw L. Slomiany
%A Amalia Slomiany
%J Open Journal of Cell Biology
%@ 2165-3909
%D 2011
%I Scientific Research Publishing
%R 10.4236/ojcb.2011.11001
%X Excessive nitric oxide generation, caused by the disturbances in nitric oxide synthase (NOS) isozyme system, plays a key role in defining the extent of gastric mucosal inflammatory response to <i>H. Pylori</i> infection. Here, we report that <i>H. Pylori</i>  LPS-induced enhancement in gastric mucosal inducible (i) iNOS expression and the impairment in constitutive (c) cNOS activity was associated with up-regulation in the inhibitory kB kinase-<i>¦Â</i> (IKK<i>¦Â</i>) activation through phosphorylation, rise in I¦ÊB-<i>¦Á</i> degradation, and the increase in the transcriptional factor, NF-¦ÊB, nuclear translocation. Further, we show that the countering effect of peptide hormone, ghrelin, on the LPS-induced disturbances in NOS isozyme system was reflected in the increase in Src/Akt-dependent cNOS activation through phosphorylation and the suppression of IKK-<i>¦Â</i> activity through cNOSmediated IKK-<i>¦Â</i> protein S-nitrosylation. As a consequence, ghrelin exerted the inhibitory effect on the LPS-induced rise in I¦ÊB-<i>¦Á</i> degradation and NF-¦ÊB nuclear translocation, thus leading to iNOS gene suppression and the repression of iNOS induction. These results point to a central role of cNOS activation in controlling the signaling pathways of the LPS-triggered iNOS gene induction. Moreover, our findings suggest a molecular mechanism by which ghrelin suppresses the gastric mucosal proinflammatory consequences of <i>H. Pylori</i>  infection.
%K H. Pylori
%K Gastric Mucosa
%K Ghrelin
%K cNOS Activation
%K IKK-¦Â S-Nitrosylation
%U http://www.scirp.org/journal/PaperInformation.aspx?PaperID=16421