Document Detail


Interleukin-31 and oncostatin-M mediate distinct signaling reactions and response patterns in lung epithelial cells.
MedLine Citation:
PMID:  17148439     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Lung epithelial cells are primary targets of oncostatin M (OSM) and, to a lower degree, of interleukin (IL)-6 and IL-31, all members of the IL-6 cytokine family. The OSM receptor (OSMR) signals through activation of STAT and mitogen-activated protein kinase pathways to induce genes encoding differentiated cell functions, reduce cell-cell interaction, and suppress cell proliferation. IL-31 functions through the heteromeric IL-31 receptor, which shares with OSMR the OSMRbeta subunit, but does not engage gp130, the common subunit of all other IL-6 cytokine receptors. Because the response of epithelial cells to IL-31 is unknown, the action of IL-31 was characterized in the human alveolar epithelial cell line A549 in which the expression of the ligand-binding IL-31Ralpha subunit was increased. IL-31 initiated signaling that differed from other IL-6 cytokines by the particularly strong recruitment of the STAT3, ERK, JNK, and Akt pathways. IL-31 was highly effective in suppressing proliferation by altering expression of cell cycle proteins, including up-regulation of p27(Kip1) and down-regulation of cyclin B1, CDC2, CDK6, MCM4, and retinoblastoma. A single STAT3 recruitment site (Tyr-721) in the cytoplasmic domain of IL-31Ralpha exerts a dominant function in the entire receptor complex and is critical for gene induction, morphological changes, and growth inhibition. The data suggest that inflammatory and immune reactions involving activated T-cells regulate functions of epithelial cells by IL-6 cytokines through receptor-defined signaling reactions.
Authors:
Souvik Chattopadhyay; Erin Tracy; Ping Liang; Olivier Robledo; Stefan Rose-John; Heinz Baumann
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2006-12-05
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  282     ISSN:  0021-9258     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2007 Feb 
Date Detail:
Created Date:  2007-01-29     Completed Date:  2007-04-10     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3014-26     Citation Subset:  IM    
Affiliation:
Department of Molecular and Cellular Biology and Cancer Genetics, Roswell Park Cancer Institute, Buffalo, New York 14263, USA.
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MeSH Terms
Descriptor/Qualifier:
Brain Neoplasms
Cell Line, Tumor
Cytokines / physiology
Genes, Reporter
Glioma
Humans
Interleukin-6 / genetics,  physiology
Interleukins / pharmacology*
Lung / immunology,  physiology*
Neuroblastoma
Oligodendroglia
Oncostatin M / pharmacology*
Receptors, Interleukin / genetics,  physiology
Receptors, Oncostatin M / genetics,  physiology
Recombinant Proteins / metabolism
Respiratory Mucosa / immunology,  physiology*
Transfection
Grant Support
ID/Acronym/Agency:
CA085580/CA/NCI NIH HHS; CA16056/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Cytokines; 0/IL31 protein, human; 0/IL31RA protein, human; 0/Interleukin-6; 0/Interleukins; 0/Receptors, Interleukin; 0/Receptors, Oncostatin M; 0/Recombinant Proteins; 106956-32-5/Oncostatin M

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


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