Document Detail


Restoration of PPARγ reverses lipid accumulation in alveolar macrophages of GM-CSF knockout mice.
MedLine Citation:
PMID:  21036914     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Pulmonary alveolar proteinosis (PAP) is a lung disease characterized by a deficiency of functional granulocyte macrophage colony-stimulating factor (GM-CSF) resulting in surfactant accumulation and lipid-engorged alveolar macrophages. GM-CSF is a positive regulator of PPARγ that is constitutively expressed in healthy alveolar macrophages. We previously reported decreased PPARγ and ATP-binding cassette transporter G1 (ABCG1) levels in alveolar macrophages from PAP patients and GM-CSF knockout (KO) mice, suggesting PPARγ and ABCG1 involvement in surfactant catabolism. Because ABCG1 represents a PPARγ target, we hypothesized that PPARγ restoration would increase ABCG1 and reduce macrophage lipid accumulation. Upregulation of PPARγ was achieved using a lentivirus expression system in vivo. GM-CSF KO mice received intratracheal instillation of lentivirus (lenti)-PPARγ or control lenti-eGFP. Ten days postinstillation, 79% of harvested alveolar macrophages expressed eGFP, demonstrating transduction. Alveolar macrophages showed increased PPARγ and ABCG1 expression after lenti-PPARγ instillation, whereas PPARγ and ABCG1 levels remained unchanged in lenti-eGFP controls. Alveolar macrophages from lenti-PPARγ-treated mice also exhibited reduced intracellular phospholipids and increased cholesterol efflux to HDL, an ABCG1-mediated pathway. In vivo instillation of lenti-PPARγ results in: 1) upregulating ABCG1 and PPARγ expression of GM-CSF KO alveolar macrophages, 2) reducing intracellular lipid accumulation, and 3) increasing cholesterol efflux activity.
Authors:
Anagha Malur; Anna D Baker; Almedia J McCoy; Greg Wells; Barbara P Barna; Mani S Kavuru; Achut G Malur; Mary Jane Thomassen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-10-29
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  300     ISSN:  1522-1504     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-20     Completed Date:  2011-01-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L73-80     Citation Subset:  IM    
Affiliation:
East Carolina Univ., Greenville, NC 27834, USA.
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MeSH Terms
Descriptor/Qualifier:
ATP-Binding Cassette Transporters / genetics,  metabolism
Animals
Cholesterol / metabolism
Granulocyte-Macrophage Colony-Stimulating Factor / deficiency,  genetics*,  physiology
Humans
Lipids / physiology
Macrophages, Alveolar / metabolism,  pathology
Mice
Mice, Knockout
PPAR gamma / genetics*,  metabolism,  therapeutic use
Pulmonary Alveolar Proteinosis / drug therapy,  genetics,  metabolism
Pulmonary Surfactants / metabolism
Chemical
Reg. No./Substance:
0/ABCG1 protein, human; 0/ATP-Binding Cassette Transporters; 0/Lipids; 0/PPAR gamma; 0/Pulmonary Surfactants; 57-88-5/Cholesterol; 83869-56-1/Granulocyte-Macrophage Colony-Stimulating Factor

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


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