Cell proliferation of estrogen-sensitive cells: the case for negative control.

Abstract

THAT the administration of estrogens to oophorectomized vertebrates results in the proliferation of certain cell types in secondary sex organs has been acknowledged for decades (1). Whether 17β-estradiol (E2) acts directly or indirectly on the proliferation of such target cells has been widely debated without reaching a conclusive answer. Since a definitive answer to this question cannot be obtained using whole animals, researchers explored models in which rodent target tissues have been explanted in culture (2–4). However, these experimental designs were not sufficiently discriminatory to conclude whether proliferation was due directly to the estrogen interaction with the cell that was stimulated or whether intermediate steps among cell types or within cells were responsible for the effect observed (1–10). During the 60's and 70's renewed interest in characterizing the proliferative response of estrogen target tissues in whole animal models became apparent as the concept of the estrogen receptor, or estr...