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

Laura J Parry, Lenka A. Vodstrcil, Anna Madden, Stephanie H. Amir, Katrina Baldwin, Mary E Wlodek, Kevin R. Nicholas

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7 Citations (Scopus)


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 β-casein and α-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 β-casein and α-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.

Original languageEnglish
Pages (from-to)549-560
Number of pages12
JournalReproduction, Fertility and Development
Issue number4
Publication statusPublished - 2009
Externally publishedYes


  • Fetal growth
  • Milk proteins

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