Milk osmolarity maintains an isotonic status for suckling infants during lactation. However, it remains unclear how the water content in milk is regulated in lactating mammary glands. In lactating mammary alveoli and ducts, mammary epithelial cells (MECs) are in direct contact with milk. In this study, we focus on two types of water channels, aquaporin 3 (AQP3) and AQP5, in alveolar and ductal MECs before and after parturition. AQP3 showed diffuse localization in the cytoplasm of ductal MECs but concentrated localization in the basolateral membrane of alveolar MECs during the late pregnancy and lactation periods. Translocation of AQP5 from the cytoplasm toward the apical membrane occurred in ductal MECs immediately before parturition. Subsequently, we examined the hormonal influences on the expression of AQP3 and AQP5 in cultured MECs in vitro. Progesterone and estrogen distinctly increased AQP3 and AQP5 in cultured MECs, respectively. Cotreatment with prolactin and dexamethasone significantly decreased both AQP3 and AQP5. Prolactin also facilitated the translocation of AQP5 into the apical membrane of MECs. In cultured MECs, AQP3 was homogeneously expressed in MECs, whereas AQP5 showed different expression levels between MECs regardless of the hormonal treatment. Different activation states of the prolactin/STAT5 pathway were also observed between ductal and alveolar MECs. These findings suggest that the expression pattern of AQP3 and AQP5 is distinctly regulated by lactogenic hormones in alveolar and ductal MECs before and after parturition. AQP5 expressed in ductal MECs may function as a water channel to regulate milk osmolarity in mice.
All Science Journal Classification (ASJC) codes