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Differential effects of insulin and dexamethasone on pulmonary surfactant-associated genes and proteins in A549 and H441 cells and lung tissue
Z. Rucka, P. Vanhara, I. Koutna, L. Tesarova, M. Potesilova, S. Stejskal, P. Simara, J. Dolezel, V. Zvonicek, O. Coufal, I. Capov,
Language English Country Greece
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Free Medical Journals
from 2006 to 1 year ago
Freely Accessible Science Journals
from 2006
ProQuest Central
from 2012-01-01
Medline Complete (EBSCOhost)
from 2013-08-01
Health & Medicine (ProQuest)
from 2012-01-01
- MeSH
- Adenocarcinoma genetics MeSH
- Dexamethasone pharmacology MeSH
- Insulin pharmacology MeSH
- Middle Aged MeSH
- Humans MeSH
- Cell Line, Tumor MeSH
- Lung Neoplasms genetics MeSH
- Lung drug effects metabolism MeSH
- Pulmonary Surfactant-Associated Protein A genetics metabolism MeSH
- Pulmonary Surfactant-Associated Protein B genetics metabolism MeSH
- Pulmonary Surfactant-Associated Protein C genetics metabolism MeSH
- Pulmonary Surfactant-Associated Protein D genetics metabolism MeSH
- Pulmonary Surfactant-Associated Proteins genetics metabolism MeSH
- Gene Expression Regulation, Neoplastic drug effects MeSH
- Gene Expression Regulation drug effects MeSH
- Aged MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
In this study, the effects of insulin and dexamethasone on the expression and mRNA transcription of 4 pulmonary surfactant-associated proteins [surfactant protein (SFTP)A, SFTPB, SFTPC and SFTPD] were examined. The commercially available cell lines, A549 and H441, were used as acceptable models of lung surfactant-producing cells. Subsequently, the effects of insulin on the expression of surfactant-associated proteins were examined in patients with lung adenocarcinoma during lung resection. Our results demonstrated the inhibitory effects of insulin on the transcription of the SFTPB, SFTPC and SFTPD genes in H441 cells and the SFTPB gene in A549 cells. Treatment with insulin significantly decreased the protein expression of SFTPA1 and SFTPA2 in the H441 cells and that of proSFTPB in the A549 cells. Dexamethasone promoted the transcription of the SFTPB, SFTPC and SFTPD genes in the A549 and H441 cells and reduced the transcription of the SFTPA1 and SFTPA2 genes in the H441 cells (SFTPA mRNA expression was not detected in A549 cells). Furthermore, we demonstrated that the mRNA levels of the selected genes were significantly lower in the cell lines compared to the lung tissue. A549 and H441 cells represent similar cell types. Yet, in our experiments, these cells reacted differently to insulin and/or dexamethasone treatment, and the mRNA levels of their main protein products, surfactant-associated proteins, were significantly lower than those in real tissue. Therefore, the results obtained in this study challenge the suitability of A549 and H441 cells as models of type II pneumocytes and Clara cells, respectively. However, we successfully demonstrate the possibility of studying the effects of insulin on pulmonary surfactant-associated genes and proteins in patients with lung adenocarcinoma.
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