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Progesterone action in normal mouse mammary gland
S Wang1, L J Counterman, S Z Haslam
1Physiology Department, Michigan State University, East Lansing 48824.
Endocrinology
|November 1, 1990
Summary
Progestins promote mammary gland growth through estrogen-dependent mechanisms in epithelial cells and distinct, estrogen-independent pathways in stromal cells. Estrogen significantly influences progestin activity by increasing progesterone receptors (PgR) in mammary epithelium.
Area of Science:
- Endocrinology
- Cell Biology
- Reproductive Biology
Background:
- Progesterone and estrogen are crucial for mammary gland development.
- Mammary progesterone receptors (PgR) are 80% estrogen-inducible in epithelium and 20% estrogen-independent in stroma.
Purpose of the Study:
- To investigate how progestins stimulate mammary growth via epithelial and stromal interactions.
- To assess the role of estrogen in mediating these progestin-stromal and progestin-epithelial interactions.
Main Methods:
- Hormone implants (progestins, estrogen) in mammary glands.
- Morphological analysis of mammary gland changes.
- Quantification of DNA synthesis in epithelial and stromal cells via DNA histoautoradiography.
Main Results:
- Progestin-induced proliferation in epithelial cells is locally mediated and estrogen-dependent, correlating with increased PgR.
- Estrogen dose, not progestin dose, was the primary determinant of progestin activity in epithelium.
- Stromal cell progestin activity was estrogen-independent, with RU486 stimulating stromal DNA synthesis, an effect augmented by estrogen.
Conclusions:
- Progestin effects on mammary epithelial cells are mediated by estrogen-dependent PgR.
- Progestin mechanisms in stromal cells differ from epithelial cells and require further elucidation.
- Estrogen plays a key role in regulating progestin-driven mammary gland growth.