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Submitted on April 21, 2004
Accepted on July 6, 2004
Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, Texas 77030, USA
* To whom correspondence should be addressed. E-mail: agoulnik{at}bcm.tmc.edu.
Relaxin (RLN) is a small peptide hormone that affects a variety of biological processes. Rln1 knockout mice exhibit abnormal nipple development, prolonged parturition, age-related pulmonary fibrosis, and abnormalities in the testis and prostate. We describe here relaxin receptor Lgr7 deficient mice. Mutant females have grossly underdeveloped nipples and are unable to feed their progeny. Some Lgr7-/- females were unable to deliver their pups. Histological analysis of Lgr7 mutant lung tissues demonstrates increased collagen accumulation and fibrosis surrounding the bronchioles and the vascular bundles, absent in wild-type animals. However, Lgr7 deficient males do not exhibit abnormalities in the testes or prostate as seen in Rln1 knockout mice. Lgr7 deficient females with additional deletion of Lgr8 (Great), another putative receptor for relaxin, are fertile and have normal sized litters. Double mutant males have normal sized prostate and testes, suggesting that Lgr8 does not account for differences in Rln1-/- and Lgr7-/- phenotypes. Transgenic overexpression of Insl3, the cognate ligand for Lgr8, does not rescue the mutant phenotype of Lgr7 deficient female mice indicating non-overlapping functions of the two receptors. Our data indicate that neither Insl3 nor Lgr8 contribute to the relaxin signaling pathway. We conclude that the Insl3/Lgr8 and Rln1/Lgr7 actions do not overlap in vivo.
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