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Howard Florey Institute of Experimental Physiology and Medicine (I.M., G.W.T., C.S.S.), University of Melbourne, Parkville, Victoria 3010, Australia; and Murdoch Children’s Research Institute (N.R.S., S.G.R., M.L.K.T.), Royal Childrens Hospital, Parkville, Victoria 3052, Australia
Address all correspondence and requests for reprints to: Associate Professor Mimi L. K. Tang, M.D., Ph.D., Department of Immunology, Murdoch Children’s Research Institute, Royal Childrens Hospital, Parkville, Victoria 3052, Australia. E-mail: mimi.tang{at}rch.org.au; or Dr. Chrishan S. Samuel, Howard Florey Institute, The University of Melbourne, Victoria 3010, Australia. E-mail: c.samuel{at}hfi.unimelb.edu.au.
We examined the relationship among relaxin (a peptide hormone that stimulates collagen degradation), airway fibrosis, other changes of airway remodeling, and airway hyperresponsiveness (AHR) in an animal model of allergic airway disease. Eight- to 10-wk-old relaxin gene-knockout (RLX–/–) and wild-type (RLX+/+) mice were sensitized with ovalbumin (OVA) or saline ip at d 0 and 14 and challenged three times per week for 6 wk with nebulized 2.5% OVA or saline. Saline-treated control RLX+/+ and RLX–/– mice had equivalent collagen expression and baseline airway responses. OVA-treated RLX–/– mice developed airway inflammation equivalent to that in OVA-treated RLX+/+ mice. However, OVA-treated RLX–/– mice had markedly increased lung collagen deposition as compared with OVA-treated RLX+/+ and saline-treated mice (all P < 0.05). Collagen was predominantly deposited in the subepithelial basement membrane region and submucosal regions in both OVA-treated RLX+/+ and RLX–/– mice. The increased collagen measured in OVA-treated RLX–/– mice was associated with reduced matrix metalloproteinase (MMP)-9 (P < 0.02) expression and failure to up-regulate matrix metalloproteinase-2 expression, compared with levels in OVA-treated RLX+/+ mice. Goblet cell numbers were equivalent in OVA-treated RLX–/– and RLX+/+ mice and increased, compared with saline-treated animals. Both OVA-treated RLX+/+ and RLX–/– mice developed similar degrees of AHR after OVA treatment. These findings demonstrate a critical role for relaxin in the inhibition of lung collagen deposition during an allergic inflammatory response. Increased deposition of collagen per se did not influence airway epithelial structure or AHR.
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  S. G. Royce, Y. R. Miao, M. Lee, C. S. Samuel, G. W. Tregear, and M. L. K. Tang Relaxin Reverses Airway Remodeling and Airway Dysfunction in Allergic Airways Disease Endocrinology, June 1, 2009; 150(6): 2692 - 2699. [Abstract] [Full Text] [PDF]
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A. Kern and G. D. Bryant-Greenwood Characterization of Relaxin Receptor (RXFP1) Desensitization and Internalization in Primary Human Decidual Cells and RXFP1-Transfected HEK293 Cells Endocrinology, May 1, 2009; 150(5): 2419 - 2428. [Abstract] [Full Text] [PDF]
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 I. Mookerjee, T. D. Hewitson, M. L. Halls, R. J. Summers, M. L. Mathai, R. A. D. Bathgate, G. W. Tregear, and C. S. Samuel Relaxin inhibits renal myofibroblast differentiation via RXFP1, the nitric oxide pathway, and Smad2 FASEB J, April 1, 2009; 23(4): 1219 - 1229. [Abstract] [Full Text] [PDF]
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C. S. Samuel, S. G. Royce, B. Chen, H. Cao, J. A. Gossen, G. W. Tregear, and M. L. K. Tang Relaxin Family Peptide Receptor-1 Protects against Airway Fibrosis during Homeostasis But Not against Fibrosis Associated with Chronic Allergic Airways Disease Endocrinology, March 1, 2009; 150(3): 1495 - 1502. [Abstract] [Full Text] [PDF]
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Q. Xu, E. D. Lekgabe, X.-M. Gao, Z. Ming, G. W. Tregear, A. M. Dart, R. A. D. Bathgate, C. S. Samuel, and X.-J. Du Endogenous Relaxin Does Not Affect Chronic Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis Endocrinology, February 1, 2008; 149(2): 476 - 482. [Abstract] [Full Text] [PDF]
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 T.-Y. Ho, W. Yan, and C. A. Bagnell Relaxin-induced matrix metalloproteinase-9 expression is associated with activation of the NF-{kappa}B pathway in human THP-1 cells J. Leukoc. Biol., May 1, 2007; 81(5): 1303 - 1310. [Abstract] [Full Text] [PDF]
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A. Kern, A. I. Agoulnik, and G. D. Bryant-Greenwood The Low-Density Lipoprotein Class A Module of the Relaxin Receptor (Leucine-Rich Repeat Containing G-Protein Coupled Receptor 7): Its Role in Signaling and Trafficking to the Cell Membrane Endocrinology, March 1, 2007; 148(3): 1181 - 1194. [Abstract] [Full Text] [PDF]
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E. D. Lekgabe, S. G. Royce, T. D. Hewitson, M. L. K. Tang, C. Zhao, X. L. Moore, G. W. Tregear, R. A. D. Bathgate, X.-J. Du, and C. S. Samuel The Effects of Relaxin and Estrogen Deficiency on Collagen Deposition and Hypertrophy of Nonreproductive Organs Endocrinology, December 1, 2006; 147(12): 5575 - 5583. [Abstract] [Full Text] [PDF]
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J. D. Silvertown, J. S. Walia, A. J. Summerlee, and J. A. Medin Functional Expression of Mouse Relaxin and Mouse Relaxin-3 in the Lung from an Ebola Virus Glycoprotein-Pseudotyped Lentivirus via Tracheal Delivery Endocrinology, August 1, 2006; 147(8): 3797 - 3808. [Abstract] [Full Text] [PDF]
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