Finally, conditionally deleting Stat5 (a and b) during pregnancy induced premature cell death, indicating that it is critical for cell survival at this developmental stage (14).Developmental studies using Northern and Western blotting of whole murine mammary gland homogenates demonstrated that Stat5a is present in both the immature and mature virgin, increases during pregnancy, and reaches a maximal level during late pregnancy and lactation (16, 17).
However, expression in the stromal and epithelial compartments could not be discriminated using these approaches, and the increase in Stat5a might therefore reflect increased epithelial cell number rather than increased expression per epithelial cell.
In addition, Western blotting does not permit one to localize expression to specific epithelial structures such as ducts, end buds, and alveoli.
The results demonstrate that Stat5a expression increases dramatically at puberty and after ovariectomy in response to the ovarian hormones E and P.
Furthermore, Stat5a extensively colocalizes with both estrogen receptors (ER) and PR, suggesting that it is a target of these receptors and may mediate some of the effects of E and P in the mammary gland.
A more recent study used immunohistochemistry to examine total Stat5 expression in mouse mammary epithelium.
They found that Stat5 was expressed in the adult virgin as well as the pregnant gland, but immature animals were not examined (18).
Several pathways for activating Stat5a have been identified, but little is known about the mechanisms that regulate its expression in this tissue.
In this report, we used immunofluorescent staining to examine Stat5a expression in mammary epithelial cells during normal development and in response to treatment with the ovarian hormones estrogen (E) and progesterone (P).
In lactating animals, Stat5a induces expression of milk protein genes, largely in response to PRL, and Stat5a activation in virgin animals also seems to be predominantly due to PRL (18).