Abstract:
:We studied ligand-receptor interactions between relaxin (RLN), insulin-like 3 peptide (INSL3), and LGR7 and LGR8 receptors. The phenotypic effects of deficiency for Lgr7 and Lgr8 receptors, transgenic overexpression of Rln1 and Insl3, and different combinations of these mutations in mice were analyzed. It was reported that Rln1-deficient mice exhibit abnormal nipple development, prolonged parturition, age-related pulmonary fibrosis, and abnormalities in the testis and prostate. Mutation of Lgr8 or its cognate ligand Insl3 causes cryptorchidism. Mutant females deficient for the Lgr7 receptor have grossly undeveloped nipples and are unable to feed their progeny. Parturition is prolonged in these females, resulting in a significantly higher number of stillborn pups. Histologic analysis of Lgr7 mutant lung tissues demonstrates increased collagen accumulation and perivenular smooth muscle hypertrophy. However, Lgr7-deficient males do not exhibit abnormalities of male reproductive organs as seen in Rln1 knockout mice. Double-mutant males deficient for Lgr7 and Lgr8 have a normal prostate, suggesting that Lgr8 does not account for differences in Rln1-/- and Lgr7-/- phenotypes. We also produced mice with transgenic overexpression of Rln1 under rat insulin 2 promoter. Rln1 transgenic females exhibited increased nipple size, whereas Rln1 transgenic females deficient in Lgr7 had undeveloped nipples, indicating that Lgr7 is the only receptor for relaxin that mediates this effect. Transgenic overexpression of Rln1 does not affect gonadal descent in females, and transgenic overexpression of Insl3 does not rescue the mutant phenotype of Lgr7-deficient mice, suggesting the non-overlapping functions of two signaling pathways. In summary, our data indicate that the Insl3/Lgr8 and Rln1/Lgr7 pathways are distinct and separate in vivo. Therefore, we propose to rename Lgr8 as Insl3r (Insl3 receptor) and Lgr7 as Rlnr (relaxin receptor).
journal_name
Ann N Y Acad Scijournal_title
Annals of the New York Academy of Sciencesauthors
Feng S,Bogatcheva NV,Kamat AA,Agoulnik AIdoi
10.1196/annals.1282.012subject
Has Abstractpub_date
2005-05-01 00:00:00pages
82-90eissn
0077-8923issn
1749-6632pii
1041/1/82journal_volume
1041pub_type
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