Premium
Progesterone increases metabolic rate and progesterone withdrawal enhances epithelial integrity of mammary epithelium
Author(s) -
Quesnell Rebecca R.,
Schultz Bruce D.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1424
Subject(s) - prolactin , epithelium , medicine , hormone , endocrinology , in vitro , biology , cell culture , mammary gland , andrology , biochemistry , cancer , breast cancer , genetics
Progesterone receptors (PR) were documented in a bovine mammary epithelial cell line (BME‐UV), which allowed us to test the hypothesis that progesterone (PRG) has direct effects on mammary epithelial function. PR were identified in BME‐UV cells at the mRNA and protein (Western blot) levels. Thus, BME‐UV cells were grown as confluent monolayers in either no added hormones, PRG, prolactin (PRL), and PRG + PRL over a 14 day culture period. Parturition was simulated in vitro by using PRG‐free medium for the final day in culture. PRG exposure caused an immediate and substantial increase in glucose utilization that was maintained for at least 10 days of continued PRG exposure. Small effects on transepithelial electrical resistance ( R te ) were identified in the presence of these hormones. However, treatment including PRG and PRL for the first 13 days of culture, but lacking PRG for the final 24 hours prior to assay substantially increased R te . The results demonstrate that PRG exposure is directly associated with an increase in mammary cell metabolism. PRG also ‘primed’ the epithelial cells for a rapid transition to greater R te when PRG was withdrawn. This suggests that PRG increases metabolic activity of mammary epithelial cells during pregnancy and that the sudden reduction in circulating PRG levels at parturition signals the rapid closure of mammary epithelial tight junctions. [USDA NRI, RRO17686 NCRR NIH Support]