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Hyperoxia regulates leukotriene (LT) receptor mRNA expression in the developing rat lung
Author(s) -
Reynolds Stephen,
Brennan Kathryn,
Olson David
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1442-c
Subject(s) - hyperoxia , lung , messenger rna , receptor , medicine , andrology , endocrinology , immunology , biology , gene , biochemistry
Hyperoxia in newborn rats inhibits alveolarization and replicates many of the features of human newborn chronic lung disease (NCLD). Hyperoxia is known to cause an increase in LT expression in the lung and previous studies have demonstrated that LT administration during alveolarization can either arrest (LTB 4 ) or accelerate (LTD 4 ) lung development, suggesting they may be key mediators of this process. Our aim was to assess whether LTB 4 receptor (BLT 1 & BLT 2 ) and LTD 4 receptor (CysLT 1 & CysLT 2 ) mRNA expression is altered by hyperoxia. Methods Rat pups were placed in a normoxic (21% O 2 ) or hyperoxic (>95% O 2 ) environment from postnatal days 4 to 14. Pups were euthanized and lungs harvested on days 4, 6, 9, 12 and 14. Lung total RNA was extracted and analyzed using Real‐Time RT‐PCR. Data were analyzed by two‐way ANOVA. Results The mRNA abundance of BLT 1 and CysLT 2 increased with age (p < 0.001) whilst BLT 2 mRNA abundance decreased (p = 0.001). Each of these effects was accelerated by hyperoxia (p < 0.001). CysLT 1 mRNA abundance also increased with time (p < 0.001) but hyperoxia generally decreased mRNA expression (p < 0.005). Conclusions All four LT receptors demonstrate clear changes in expression during alveolarization supporting the findings of previous research showing that LTs are involved in this process. The present study is the first to show that hyperoxia affects pulmonary LT receptor levels, suggesting that LTs are involved in the disruption of alveolarization caused by high oxygen concentrations and could be linked to NCLD. Supported by the Canadian Institutes of Health Research and the Hospital for Sick Children Foundation.