Document Detail


Effect of alveolar epithelial cell plasticity on the regulation of GM-CSF expression.
MedLine Citation:
PMID:  22227205     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Local pulmonary expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) is critically important for defense of the pulmonary alveolar space. It is required for surfactant homeostasis and pulmonary innate immune responses and is protective against lung injury and aberrant repair. Alveolar epithelial cells (AEC) are a major source of GM-CSF; however, the control of homeostatic expression of GM-CSF is incompletely characterized. Increasing evidence suggests considerable plasticity of expression of AEC phenotypic characteristics. We tested the hypothesis that this plasticity extends to regulation of expression of GM-CSF using 1) MLE-12 cells (a commonly used murine cell line expressing some features of normal type II AEC, 2) primary murine AEC incubated under standard conditions [resulting in rapid spreading and loss of surfactant protein C (SP-C) expression with induction of the putative type I cell marker (T1α)], or 3) primary murine AEC on a hyaluronic acid/collagen matrix in defined medium, resulting in preservation of SP-C expression. AEC in standard cultures constitutively express abundant GM-CSF, with further induction in response to IL-1β but little response to TNF-α. In contrast, primary cells cultured to preserve SP-C expression and MLE-12 cells both express little GM-CSF constitutively, with significant induction in response to TNF-α and limited response to IL-1β. We conclude that constitutive and cytokine-induced expression of GM-CSF by AEC varies in concert with other cellular phenotypic characteristics. These changes may have important implications both for the maintenance of normal pulmonary homeostasis and for the process of repair following lung injury.
Authors:
Mustafa Mir-Kasimov; Anne Sturrock; Michael McManus; Robert Paine
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2012-01-06
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  302     ISSN:  1522-1504     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-03-16     Completed Date:  2012-07-16     Revised Date:  2012-08-30    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L504-11     Citation Subset:  IM    
Affiliation:
Department of Veterans Affairs Medical Center, University of Utah School of Medicine, Salt Lake City, 84132, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Line
Collagen / metabolism
Culture Media
Epithelial Cells / cytology,  metabolism
Granulocyte-Macrophage Colony-Stimulating Factor / biosynthesis*,  genetics,  metabolism
Homeostasis
Hyaluronic Acid / metabolism
Interleukin-1beta / metabolism
Lung Injury / genetics,  metabolism
Membrane Glycoproteins / genetics
Mice
Mice, Inbred C57BL
Peptides / genetics
Pulmonary Alveoli / cytology,  metabolism*
Tumor Necrosis Factor-alpha / metabolism
Chemical
Reg. No./Substance:
0/Culture Media; 0/Gp38 protein, mouse; 0/Interleukin-1beta; 0/Membrane Glycoproteins; 0/Peptides; 0/Sftpc protein, mouse; 0/Tumor Necrosis Factor-alpha; 83869-56-1/Granulocyte-Macrophage Colony-Stimulating Factor; 9004-61-9/Hyaluronic Acid; 9007-34-5/Collagen

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


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