Uncertainties in the current understanding of gas exchange in spontaneous pneumothorax: effective lung ventilation may persist in a smaller-sized pneumothorax

Subotic, Dragan; Mandaric, D.; Gajić, M; Vukcevic, M.

doi:10.1016/j.mehy.2004.12.012

Cited by 2 publications

(3 citation statements)

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“…During the pneumothorax condition and treatment, atelectasis and reexpansion are associated with acute alveolar hypoxia and reoxygenation, respectively [12]. We found induced expression of HIF-1α, a transcription factor involved in hypoxia signaling events, and it co-localized with HO-1 in macrophages from PSP-S patients.…”

Section: Discussionmentioning

confidence: 70%

“…Since hypoxia/reoxygenation alone without CS exposure did not induce HIF-1α in macrophages of PSP-NS patients, our data suggest that CS preconditioning is required for the hypoxia/reoxygenation induction of HIF-1α expression. Such a relationship was further supported by in vitro experiments in macrophages exposed to CS then hypoxia and reoxygenation, to mimic conditions occurring during the pneumothorax condition and treatment in smokers [12]. In these experiments, HO-1 induction was suppressed by selective HIF-1α gene silencing.…”

Section: Discussionmentioning

confidence: 78%

“…During the pneumothorax condition and treatment, atelectasis and reexpansion are associated with acute alveolar hypoxia and reoxygenation, respectively [12]. Therefore, our second aim was to examine the mechanism(s) involved in inducing HO-1, BVR and H-ferritin expression in PSP by analyzing the expression of and the roles of transcription factors involved in signaling events after hypoxia/reoxygenation and/or cigarette smoke exposure in the aforementioned lung biopsies and in vitro in a human monocyte/macrophage cell line (THP-1).…”

Section: Introductionmentioning

confidence: 99%

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Induction of Heme Oxygenase-1, Biliverdin Reductase and H-Ferritin in Lung Macrophage in Smokers with Primary Spontaneous Pneumothorax: Role of HIF-1α

et al. 2010

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BackgroundFew 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-1α, 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 FindingsmRNA 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-1α 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-1α nuclear translocation was responsible for HO-1, BVR and H-ferritin induction mediated by CS and hypoxia/reoxygenation.Conclusions/SignificancePSP in smokers is associated with lung macrophage oxidative stress. The response to this condition involves HIF-1α-mediated induction of HO-1, BVR and H-ferritin.

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Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 99%

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