| Effect of alveolar epithelial cell plasticity on the regulation of GM-CSF expression. | |
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MedLine Citation:
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PMID: 22227205 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Mustafa Mir-Kasimov; Anne Sturrock; Michael McManus; Robert Paine |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, Non-P.H.S. Date: 2012-01-06 |
Journal Detail:
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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:
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Created Date: 2012-03-16 Completed Date: 2012-07-16 Revised Date: 2012-08-30 |
Medline Journal Info:
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Nlm Unique ID: 100901229 Medline TA: Am J Physiol Lung Cell Mol Physiol Country: United States |
Other Details:
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Languages: eng Pagination: L504-11 Citation Subset: IM |
Affiliation:
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Department of Veterans Affairs Medical Center, University of Utah School of Medicine, Salt Lake City, 84132, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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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