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Regulator of G-protein signaling 4 suppresses LPS-induced MUC5AC overproduction in the airway

Authors
 Kyoung Seob Song  ;  Hyun Jun Kim  ;  Kyubo Kim  ;  Jeung Gweon Lee  ;  Joo-Heon Yoon 
Citation
 AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol.41(1) : 40-49, 2009 
Journal Title
 AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY 
ISSN
 1044-1549 
Issue Date
2009
MeSH
Adenosine Triphosphate/metabolism ; Animals ; Cells, Cultured ; Epithelial Cells/drug effects* ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; GTP-Binding Protein alpha Subunits, Gq-G11/metabolism ; Humans ; Lipopolysaccharides/isolation & purification ; Lipopolysaccharides/pharmacology* ; Metaplasia ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mucin 5AC/genetics ; Mucin 5AC/metabolism* ; Nasal Mucosa/drug effects ; Nasal Mucosa/metabolism ; Pseudomonas aeruginosa/chemistry ; RGS Proteins/deficiency ; RGS Proteins/genetics ; RGS Proteins/metabolism* ; RNA, Messenger/metabolism ; Receptors, Purinergic P2/drug effects ; Receptors, Purinergic P2/metabolism ; Receptors, Purinergic P2Y2 ; Respiratory Mucosa/drug effects* ; Respiratory Mucosa/metabolism ; Respiratory Mucosa/pathology ; Time Factors ; Toll-Like Receptor 4/drug effects ; Toll-Like Receptor 4/metabolism ; Transfection ; Up-Regulation
Keywords
lipopolysaccharide ; ATP ; MUC5AC ; P2Y2 ; RGS4
Abstract
Mucus overproduction and airway obstruction are common features in airway mucosal inflammation. The mechanism by which LPS induces MUC5AC overexpression, however, has not been fully explored. The aims of this study were twofold: first, to examine the ATP-dependent mechanism by which LPS induces MUC5AC gene expression, and second, to identify specific molecules that could suppress LPS-induced MUC5AC expression at a G-protein-coupled receptor level. Here, we suggest that LPS from Pseudomonas aeruginosa induces MUC5AC overproduction by both an ATP-dependent pathway and an ATP-independent pathway. In addition, we showed that Regulator of G-protein signaling (RGS) 4 plays as a suppressor for ATP-induced MUC5AC expression by interacting with G alpha q in a GTP-dependent manner in vivo. These results give additional insights into the molecular mechanism of negative regulation of mucin overproduction and enhance our understanding of mucus hypersecretion during airway mucosal inflammation.
Full Text
http://www.atsjournals.org/doi/abs/10.1165/rcmb.2008-0280OC?journalCode=ajrcmb
DOI
10.1165/rcmb.2008-0280OC
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학교실) > 1. Journal Papers
5. Research Institutes (연구소) > Airway Hucus Institute (기도점액연구소) > 1. Journal Papers
Yonsei Authors
Kim, Kyu Bo(김규보)
Kim, Hyun Jun(김현준)
Song, Kyoung Seob(송경섭)
Yoon, Joo Heon(윤주헌)
Lee, Jeung Gweon(이정권)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/103924
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