Journal
ENDOCRINOLOGY
Volume 150, Issue 6, Pages 2692-2699Publisher
ENDOCRINE SOC
DOI: 10.1210/en.2008-1457
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Funding
- National Health & Medical Research Council of Australia Senior Principal Research Fellowship
- Australian Research Council Linkage Grant [LP0560620]
- National Health and Medical Research Council [546428]
- Murdoch Children's Research Institute
- Australian Research Council [LP0560620] Funding Source: Australian Research Council
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Mice deficient in the antifibrotic hormone relaxin develop structural changes in the airway that resemble airway remodeling, and demonstrate exaggerated remodeling changes in models of allergic airways disease (AAD). Relaxin expression in asthma has not been previously studied. We evaluated the efficacy of relaxin in the treatment of established airway remodeling in a mouse model of AAD. Relaxin expression in mouse AAD was also examined by immunohistochemistry and real-time PCR. BALB/c mice with established AAD were treated with relaxin or vehicle control (sc for 14 d), and effects on airway remodeling, airway inflammation, and airway hyperresponsiveness (AHR) were assessed. Relaxin expression was significantly reduced in the airways of mice with AAD compared with controls. Recombinant relaxin treatment in a mouse model of AAD reversed collagen deposition and epithelial thickening, and significantly improved AHR (all P < 0.05 vs. vehicle control), but did not influence airway inflammation or goblet cell hyperplasia. Relaxin treatment was associated with increased matrix metalloproteinase-2 levels, suggesting a possible mechanism for its antifibrotic effects. Endogenous relaxin expression is decreased in murine AAD, whereas exogenous relaxin represents a novel treatment capable of reversing established airway remodeling and AHR. (Endocrinology 150: 2692-2699, 2009)
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