Ghrelin Protects against the Detrimental Consequences of Porphyromonas gingivalis-Induced Akt Inactivation through S-Nitrosylation on Salivary Mucin Synthesis

Disturbances in nitric oxide synthase isozyme system and the impairment in salivary mucin synthesis are well-recognized features associated with oral mucosal inflammatory responses to periodontopathic bacterium, P. gingivalis. In this study, using rat sublingual gland acinar cells, we report that P....

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Main Authors: Bronislaw L. Slomiany, Amalia Slomiany
Format: Article
Language:English
Published: Wiley 2011-01-01
Series:International Journal of Inflammation
Online Access:http://dx.doi.org/10.4061/2011/807279
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author Bronislaw L. Slomiany
Amalia Slomiany
author_facet Bronislaw L. Slomiany
Amalia Slomiany
author_sort Bronislaw L. Slomiany
collection DOAJ
description Disturbances in nitric oxide synthase isozyme system and the impairment in salivary mucin synthesis are well-recognized features associated with oral mucosal inflammatory responses to periodontopathic bacterium, P. gingivalis. In this study, using rat sublingual gland acinar cells, we report that P. gingivalis LPS-induced impairment in mucin synthesis and associated suppression in Akt kinase activity were accompanied by a decrease in constitutive nitric oxide synthase (cNOS) activity and an induction in inducible nitric oxide synthase (iNOS) expression. The LPS effect on Akt inactivation was manifested in the kinase S-nitrosylation and a decrease in its phosphorylation at Ser473. Further, we demonstrate that a peptide hormone, ghrelin, countered the LPS-induced impairment in mucin synthesis. This effect of ghrelin was reflected in the suppression of iNOS and the increase in Akt activation, associated with the loss in S-nitrosylation and the increase in phosphorylation, as well as cNOS activation through phosphorylation. Our findings suggest that induction in iNOS expression by P. gingivalis-LPS leads to Akt kinase inactivation through S-nitrosylation that detrimentally impacts cNOS activation through phosphorylation as well as mucin synthesis. We also show that the countering effect of ghrelin on P. gingivalis-induced impairment in mucin synthesis is associated with Akt activation through phosphorylation.
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spelling doaj-art-afd0b6ce8e974250823b21fd053472f52025-02-03T06:42:01ZengWileyInternational Journal of Inflammation2042-00992011-01-01201110.4061/2011/807279807279Ghrelin Protects against the Detrimental Consequences of Porphyromonas gingivalis-Induced Akt Inactivation through S-Nitrosylation on Salivary Mucin SynthesisBronislaw L. Slomiany0Amalia Slomiany1Research Center, University of Medicine and Dentistry of New Jersey, P.O. Box 1709, Newark, NJ 07103-2400, USAResearch Center, University of Medicine and Dentistry of New Jersey, P.O. Box 1709, Newark, NJ 07103-2400, USADisturbances in nitric oxide synthase isozyme system and the impairment in salivary mucin synthesis are well-recognized features associated with oral mucosal inflammatory responses to periodontopathic bacterium, P. gingivalis. In this study, using rat sublingual gland acinar cells, we report that P. gingivalis LPS-induced impairment in mucin synthesis and associated suppression in Akt kinase activity were accompanied by a decrease in constitutive nitric oxide synthase (cNOS) activity and an induction in inducible nitric oxide synthase (iNOS) expression. The LPS effect on Akt inactivation was manifested in the kinase S-nitrosylation and a decrease in its phosphorylation at Ser473. Further, we demonstrate that a peptide hormone, ghrelin, countered the LPS-induced impairment in mucin synthesis. This effect of ghrelin was reflected in the suppression of iNOS and the increase in Akt activation, associated with the loss in S-nitrosylation and the increase in phosphorylation, as well as cNOS activation through phosphorylation. Our findings suggest that induction in iNOS expression by P. gingivalis-LPS leads to Akt kinase inactivation through S-nitrosylation that detrimentally impacts cNOS activation through phosphorylation as well as mucin synthesis. We also show that the countering effect of ghrelin on P. gingivalis-induced impairment in mucin synthesis is associated with Akt activation through phosphorylation.http://dx.doi.org/10.4061/2011/807279
spellingShingle Bronislaw L. Slomiany
Amalia Slomiany
Ghrelin Protects against the Detrimental Consequences of Porphyromonas gingivalis-Induced Akt Inactivation through S-Nitrosylation on Salivary Mucin Synthesis
International Journal of Inflammation
title Ghrelin Protects against the Detrimental Consequences of Porphyromonas gingivalis-Induced Akt Inactivation through S-Nitrosylation on Salivary Mucin Synthesis
title_full Ghrelin Protects against the Detrimental Consequences of Porphyromonas gingivalis-Induced Akt Inactivation through S-Nitrosylation on Salivary Mucin Synthesis
title_fullStr Ghrelin Protects against the Detrimental Consequences of Porphyromonas gingivalis-Induced Akt Inactivation through S-Nitrosylation on Salivary Mucin Synthesis
title_full_unstemmed Ghrelin Protects against the Detrimental Consequences of Porphyromonas gingivalis-Induced Akt Inactivation through S-Nitrosylation on Salivary Mucin Synthesis
title_short Ghrelin Protects against the Detrimental Consequences of Porphyromonas gingivalis-Induced Akt Inactivation through S-Nitrosylation on Salivary Mucin Synthesis
title_sort ghrelin protects against the detrimental consequences of porphyromonas gingivalis induced akt inactivation through s nitrosylation on salivary mucin synthesis
url http://dx.doi.org/10.4061/2011/807279
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