ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
PGI synthase overexpression protects against bleomycin-induced mortality and is associated with increased Nqo 1 expression.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Prostaglandins in asthma and allergic diseases.Pharmacology & therapeutics · 2019Review
- Endogenous PGIProstaglandins & other lipid mediators · 2018Article
- Prostaglandin I2 Signaling and Inhibition of Group 2 Innate Lymphoid Cell Responses.American journal of respiratory and critical care medicine · 2016Article
- The role of prostaglandins in allergic lung inflammation and asthma.Expert review of respiratory medicine · 2015Review
- Functional prostacyclin synthase promoter polymorphisms. Impact in pulmonary arterial hypertension.American journal of respiratory and critical care medicine · 2014Article
- Downregulation of NOX4 expression by roflumilast N-oxide reduces markers of fibrosis in lung fibroblasts.Mediators of inflammation · 2013Article
- PGI2 as a regulator of inflammatory diseases.Mediators of inflammation · 2012Review
- Orotracheal treprostinil administration attenuates bleomycin-induced lung injury, vascular remodeling, and fibrosis in mice.Pulmonary circulationArticle
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
The mortality rate for acute lung injury (ALI) is reported to be between 35-40%, and there are very few treatment strategies that improve the death rate from this condition. Previous studies have suggested that signaling through the prostaglandin (PG) I(2) receptor may protect against bleomycin-induced ALI in mice. We found that mice that overexpress PGI synthase (PGIS) in the airway epithelium were significantly protected against bleomycin-induced mortality and had reduced parenchymal consolidation, apoptosis of lung tissue, and generation of F(2)-isoprostanes compared with littermate wild-type controls. In addition, we show for the first time in both in vivo and in vitro experiments that PGI(2) induced the expression of NADP (H): quinoneoxidoreductase 1 (Nqo 1), an enzyme that prevents the generation of reactive oxygen species. PGI(2) induction of Nqo 1 provides a possible novel mechanism by which this prostanoid protects against bleomycin-induced mortality and identifies a potential therapeutic target for human ALI.
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