| TNF-alpha, PDGF, and TGF-beta(1) expression by primary mouse bronchiolar-alveolar epithelial and mesenchymal cells: tnf-alpha induces TGF-beta(1). | |
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MedLine Citation:
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PMID: 11502094 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The bronchiolar-alveolar epithelium (BAE) is a primary target site for inhaled agents that cause lung injury. These cells, consequently, release a broad range of mediators that influence other cell populations, including interstitial lung fibroblasts that are central to the development of interstitial pulmonary fibrosis (IPF). A number of peptide growth factors (GF) have been postulated to be essential in the pathogenesis of IPF. We demonstrate here that primary populations of mouse BAE and mesenchymal cells, maintained in culture, synthesize four potent GF. These are platelet-derived growth factor isoforms (PDGF) A and B, transforming growth factor beta-1 (TGF-beta(1)), and tumor necrosis factor alpha (TNF-alpha). A mouse lung epithelial cell isolation technique pioneered in this laboratory has been used to purify the BAE cells to greater than 85% (80 +/- 5.6% alveolar type II and 9 +/- 2.3% Clara cells) in culture. Northern analysis, RNase protection assay, and immunocytochemistry (ICC) were used to establish mRNA and protein expression of the GF over time in the cultured BAE and mesenchymal cells. We show for the first time in these primary mouse lung cells that treatment of both cell types with TNF-alpha upregulates expression of TGF-beta(1). The four GF are produced by both epithelial and mesenchymal cells but with different temporal patterns. TGF-beta(1) is expressed constitutively by BAE and mesenchymal cells, whereas TNF-alpha expression wanes over time. The findings by ICC were consistent with levels of mRNA expression in both cell types. As genetically defined and altered mouse strains are becoming increasingly valuable for modeling lung disease, studying the gene expression patterns of target cells from these animals in vitro would be useful in sorting out the complex responses by individual cell types of the lung and the interactions among the multitude of mediators that are released during lung cell injury. |
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Authors:
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G S Warshamana; M Corti; A R Brody |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Experimental and molecular pathology Volume: 71 ISSN: 0014-4800 ISO Abbreviation: Exp. Mol. Pathol. Publication Date: 2001 Aug |
Date Detail:
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Created Date: 2001-08-14 Completed Date: 2001-10-11 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0370711 Medline TA: Exp Mol Pathol Country: United States |
Other Details:
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Languages: eng Pagination: 13-33 Citation Subset: IM |
Copyright Information:
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Copyright 2001 Academic Press. |
Affiliation:
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Lung Biology Program, Tulane University Health Sciences Center, New Orleans, Louisiana 70112, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Bronchi / cytology*, immunology Cell Culture Techniques / methods Cell Survival / drug effects Cells, Cultured Fibroblasts / cytology, immunology Gene Expression Regulation / drug effects, immunology* Immunohistochemistry Kinetics Male Mesoderm / cytology, immunology Mice Mice, Inbred C57BL Organ Specificity Platelet-Derived Growth Factor / genetics* Protein Biosynthesis Pulmonary Alveoli / cytology*, immunology RNA, Messenger / genetics Respiratory Mucosa / cytology, immunology* Time Factors Transcription, Genetic Transforming Growth Factor beta / genetics*, pharmacology Tumor Necrosis Factor-alpha / genetics*, pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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NRSA HL09691-01/NR/NINR NIH HHS; R01 ES60766/ES/NIEHS NIH HHS; R01 HL60532/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Platelet-Derived Growth Factor; 0/RNA, Messenger; 0/Transforming Growth Factor beta; 0/Tumor Necrosis Factor-alpha |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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