Document Detail


Ghrelin Protects against the Detrimental Consequences of Porphyromonas gingivalis-Induced Akt Inactivation through S-Nitrosylation on Salivary Mucin Synthesis.
MedLine Citation:
PMID:  21603133     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Abstract/OtherAbstract:
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 Ser(473). 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.
Authors:
Bronislaw L Slomiany; Amalia Slomiany
Related Documents :
2173173 - Effects of ischemia on multifunctional calcium/calmodulin-dependent protein kinase type...
20149843 - Hydrogen sulfide protects neurons against hypoxic injury via stimulation of atp-sensiti...
18196973 - C-myc protein is degraded in response to uv irradiation.
Publication Detail:
Type:  Journal Article     Date:  2011-04-06
Journal Detail:
Title:  International journal of inflammation     Volume:  2011     ISSN:  2042-0099     ISO Abbreviation:  Int J Inflam     Publication Date:  2011  
Date Detail:
Created Date:  2011-05-23     Completed Date:  2011-07-14     Revised Date:  2011-07-28    
Medline Journal Info:
Nlm Unique ID:  101538188     Medline TA:  Int J Inflam     Country:  England    
Other Details:
Languages:  eng     Pagination:  807279     Citation Subset:  -    
Affiliation:
Research Center, University of Medicine and Dentistry of New Jersey, P.O. Box 1709, Newark, NJ 07103-2400, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Models for LRRK2-Linked Parkinsonism.
Next Document:  Acute arterial thrombosis after covered stent exclusion of bleeding mycotic pseudoaneurysm: treatmen...