Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 2692 - 2699 |
| Number of pages | 8 |
| Journal | Endocrinology |
| Volume | 150 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 2009 |
| Externally published | Yes |
Cite this
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Relaxin reverses airway remodeling and airway dysfunction in allergic airways disease. / Royce, Simon; Miao, Yu; Lee, Melissa; Samuel, Chrishan; Tregear, Geoffrey; Tang, Mimi.
In: Endocrinology, Vol. 150, No. 6, 2009, p. 2692 - 2699.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Relaxin reverses airway remodeling and airway dysfunction in allergic airways disease
AU - Royce, Simon
AU - Miao, Yu
AU - Lee, Melissa
AU - Samuel, Chrishan
AU - Tregear, Geoffrey
AU - Tang, Mimi
PY - 2009
Y1 - 2009
N2 - 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.
AB - 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.
UR - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=19213838
U2 - 10.1210/en.2008-1457
DO - 10.1210/en.2008-1457
M3 - Article
VL - 150
SP - 2692
EP - 2699
JO - Endocrinology
JF - Endocrinology
SN - 0013-7227
IS - 6
ER -