Document Detail


Expression analysis of Akt and MAPK signaling pathways in lung tissue of patients with idiopathic pulmonary fibrosis (IPF).
MedLine Citation:
PMID:  20536315     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE OF THE STUDY: Several studies in patients with lung cancer have shown that epidermal growth factor receptor regulates various tumorigenic processes through the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin and Ras/Raf/Mek/Erk (mitogen-activated protein kinase (MAPK)) signalling pathways. The aim of our study is to evaluate whether these pathways are implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and to seek indirect evidence of a common pathogenetic pathway with lung cancer. m-RNA expression of oncogenes participating in these two signaling pathways, as well as the combined m-RNA expression of the suppressor genes R-kip and p53 in lung tissue of patients with IPF were evaluated.
BASIC PROCEDURES: The study population was composed by two distinct groups. Patients with IPF (n = 25) and control subjects who underwent thoracic surgery for reasons other than interstitial lung disease (n = 10). Expression analysis of the aforementioned oncogenes and suppressor genes was performed using real-time reverse transcription polymerase chain reaction.
MAIN FINDINGS: We found no difference in the overall m- RNA expression between controls and IPF in both investigated pathways. However, Braf has been overexpressed in IPF samples (P = 0.01) in contrast with K-ras that has been found downregulated (P < 0.001) in comparison with controls.
PRINCIPAL CONCLUSIONS: These findings cannot exclude the hypothesis of involvement of Akt and MAPK signalling pathways in pathogenesis of IPF. However, further investigation is needed in order to verify these data.
Authors:
Katerina M Antoniou; George A Margaritopoulos; Giannoula Soufla; Emmanouil Symvoulakis; Evi Vassalou; Rena Lymbouridou; Katerina D Samara; Dimitra Kappou; Demetrios A Spandidos; Nikolaos M Siafakas
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of receptor and signal transduction research     Volume:  30     ISSN:  1532-4281     ISO Abbreviation:  J. Recept. Signal Transduct. Res.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-12     Completed Date:  2010-12-07     Revised Date:  2012-06-21    
Medline Journal Info:
Nlm Unique ID:  9509432     Medline TA:  J Recept Signal Transduct Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  262-9     Citation Subset:  IM    
Affiliation:
Department of Thoracic Medicine, Interstitial Lung Disease Unit, Medical School, University of Crete, Heraklion, Crete, Greece. katerinaantoniou@yahoo.gr
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Case-Control Studies
DNA Mutational Analysis
Demography
Female
Gene Expression Regulation
Humans
Idiopathic Pulmonary Fibrosis / enzymology*,  pathology*,  physiopathology
Lung / enzymology*,  pathology*,  physiopathology
MAP Kinase Signaling System* / genetics
Male
Middle Aged
Mitogen-Activated Protein Kinases / genetics,  metabolism*
Phosphatidylethanolamine Binding Protein / genetics,  metabolism
Proto-Oncogene Proteins B-raf / genetics,  metabolism
Proto-Oncogene Proteins c-akt / genetics,  metabolism*
Spirometry
Tumor Suppressor Protein p53 / genetics,  metabolism
ras Proteins / genetics,  metabolism
Chemical
Reg. No./Substance:
0/PEBP1 protein, human; 0/Phosphatidylethanolamine Binding Protein; 0/Tumor Suppressor Protein p53; EC 2.7.11.1/BRAF protein, human; EC 2.7.11.1/Proto-Oncogene Proteins B-raf; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 3.6.5.2/ras Proteins

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


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