A Rat Endometrial Cell Line (R1-49E1) Expressing Estrogen Receptor-α Regulated by The Tet-Off System

Background ens exert profound effects on target tissues. These effects are mediated by two estrogen receptors (ERα and ERβ) that bind to specific DNA sequences in estrogen-dependent genes. Other molecules such as growth factors, transcription factors and some oncoproteins might interact with the estrogen receptors and thus regulate the transcription of these genes. Currently there is no adequate cellular model to study these interactions. s nsfected the human wild-type ERα to an ER-negative rat epithelial endometrial cell line (Rentr01) using a tetracycline-regulated gene expression system. The exogenous receptor was correctly translated, had an appropriate hormone-binding affinity, and bound well to estrogen response elements containing DNA. s ained a new stable cell line that is ERβ negative but ERα positive (R1-49E1). The expression of receptor α can be regulated in a dose-response manner by addition of tetracycline in the culture medium. Estradiol treatment of ERα-containing cells apparently diminished cellular proliferation, and the exogenous receptor can induce the transcription of the endogenous progesterone receptor isoform B (PgR-B) gene. sions pithelial cellular model may be useful to study the interaction between estrogens and other cell signaling pathways in epithelial endometrial cell physiology.