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Publication : Normal mammary gland growth and lactation capacity in pregnant relaxin-deficient mice.

First Author  Parry LJ Year  2009
Journal  Reprod Fertil Dev Volume  21
Issue  4 Pages  549-60
PubMed ID  19383261 Mgi Jnum  J:150605
Mgi Id  MGI:3851064 Doi  10.1071/RD08243
Citation  Parry LJ, et al. (2009) Normal mammary gland growth and lactation capacity in pregnant relaxin-deficient mice. Reprod Fertil Dev 21(4):549-60
abstractText  Pups born to mice with a targeted deletion of relaxin or its receptor (Rxfp1) die within 24 h postpartum. This has been attributed, in part, to abnormal mammary gland development in relaxin-mutant mice (Rln-/-). However, mammary development is normal in relaxin receptor-mutant (Rxfp1-/-) mice. The present study aimed to verify the mammary phenotypes in late pregnant and early lactating Rln-/- mice and to test the hypothesis that relaxin is involved in milk protein synthesis. Comparisons between late pregnant and early lactating wildtype (Rln+/+) and Rln-/- mice showed no differences in lobuloalveolar structure or ductal branching in the mammary gland. Mammary explants from Rln-/- mice also expressed beta-casein and alpha-lactalbumin in response to lactogenic hormones at a similar level to Rln+/+ mice, implying normal milk protein synthesis. Pregnant Rln-/- mice infused with relaxin for 6 days gave birth to live pups without difficulty, and 96% of pups survived beyond 7 days. This is in contrast with the 100% pup mortality in saline-treated Rln-/- mice or 3-day relaxin-treated Rln-/- mice. Pups born to relaxin-treated Rln-/- dams weighed significantly less than Rln+/+ pups but had similar growth rates as their wildtype counterparts. In summary, relaxin is not critical for mammary gland development or beta-casein and alpha-lactalbumin expression in late pregnant mice. In addition, Rln-/- dams did not need to be treated with relaxin postpartum for the pups to survive, suggesting that relaxin has no role in the maintenance of lactation in mice.
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