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http://purl.uniprot.org/citations/20526373http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20526373http://www.w3.org/2000/01/rdf-schema#comment"

Background

Few data concern the pathophysiology of primary spontaneous pneumothorax (PSP), which is associated with alveolar hypoxia/reoxygenation. This study tested the hypothesis that PSP is associated with oxidative stress in lung macrophages. We analysed expression of the oxidative stress marker 4-HNE; the antioxidant and anti-inflammatory proteins heme oxygenase-1 (HO-1), biliverdin reductase (BVR) and heavy chain of ferritin (H-ferritin); and the transcription factors controlling their expression Nrf2 and HIF-1alpha, in lung samples from smoker and nonsmoker patients with PSP (PSP-S and PSP-NS), cigarette smoke being a risk factor of recurrence of the disease.

Methodology/principal findings

mRNA was assessed by RT-PCR and proteins by western blot, immunohistochemistry and confocal laser analysis. 4-HNE, HO-1, BVR and H-ferritin were increased in macrophages from PSP-S as compared to PSP-NS and controls (C). HO-1 increase was associated with increased expression of HIF-1alpha mRNA and protein in alveolar macrophages in PSP-S patients, whereas Nrf2 was not modified. To understand the regulation of HO-1, BVR and H-ferritin, THP-1 macrophages were exposed to conditions mimicking conditions in C, PSP-S and PSP-NS patients: cigarette smoke condensate (CS) or air exposure followed or not by hypoxia/reoxygenation. Silencing RNA experiments confirmed that HIF-1alpha nuclear translocation was responsible for HO-1, BVR and H-ferritin induction mediated by CS and hypoxia/reoxygenation.

Conclusions/significance

PSP in smokers is associated with lung macrophage oxidative stress. The response to this condition involves HIF-1alpha-mediated induction of HO-1, BVR and H-ferritin."xsd:string
http://purl.uniprot.org/citations/20526373http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0010886"xsd:string
http://purl.uniprot.org/citations/20526373http://purl.uniprot.org/core/author"Goven D."xsd:string
http://purl.uniprot.org/citations/20526373http://purl.uniprot.org/core/author"Boutten A."xsd:string
http://purl.uniprot.org/citations/20526373http://purl.uniprot.org/core/author"Boczkowski J."xsd:string
http://purl.uniprot.org/citations/20526373http://purl.uniprot.org/core/author"Soler P."xsd:string
http://purl.uniprot.org/citations/20526373http://purl.uniprot.org/core/author"Bonay M."xsd:string
http://purl.uniprot.org/citations/20526373http://purl.uniprot.org/core/author"Lecon-Malas V."xsd:string
http://purl.uniprot.org/citations/20526373http://purl.uniprot.org/core/author"Marchal-Somme J."xsd:string
http://purl.uniprot.org/citations/20526373http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20526373http://purl.uniprot.org/core/name"PLoS One"xsd:string
http://purl.uniprot.org/citations/20526373http://purl.uniprot.org/core/pages"e10886"xsd:string
http://purl.uniprot.org/citations/20526373http://purl.uniprot.org/core/title"Induction of heme oxygenase-1, biliverdin reductase and H-ferritin in lung macrophage in smokers with primary spontaneous pneumothorax: role of HIF-1alpha."xsd:string
http://purl.uniprot.org/citations/20526373http://purl.uniprot.org/core/volume"5"xsd:string
http://purl.uniprot.org/citations/20526373http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/20526373
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