Neonatal estradiol exposure alters uterine morphology and endometrial transcriptional activity in prepubertal gilts.

Porcine endometrial development between birth (postnatal day = PND 0) and PND 56 involves differentiation of glandular epithelium (GE) from luminal epithelium (LE) and estrogen receptor-alpha (ER) expression. Juvenile ER architecture evolves after birth, as stroma and nascent GE first express ER. Mature ER architecture is evident after PND 30, when stroma, GE and LE are ER-positive. When administered during discrete periods between PND 0 and 56, effects of estradiol-17beta valerate (EV) on the neonatal porcine uterus relate to endometrial ER architecture. Transient EV exposure from birth reduces embryo survival in pregnant adult gilts. Effects of EV, administered as juvenile endometrial ER architecture develops (P1, PND 0-13), or after mature ER architecture is established (P2, PND 42-55), were evaluated in uteri from gilts treated with corn oil or EV in P1 or P2 and hysterectomized on PND 100 without additional steroids (NSt), on PND 102 after EV on PND100-101 (EV2), or on PND 117 after EV2 followed by progesterone on PND 102-116 (EP). Neonatal EV reduced uterine weight (P < 0.02), size (P < 0.01), luminal protein content (P < 0.07), and percent incorporation of 3H-leucine into nondialyzable endometrial products in vitro (P < 0.01). Group (NSt, EV2, EP) -specific treatment effects detected for endometrial ER, progesterone receptor, uteroferrin, and/or retinol binding protein mRNA levels were frequently related to period (P1,P2). Results support the idea that estrogen-sensitive postnatal organizational events, including those defined, in part, by endometrial ER architecture, are likely components of genetic and epigenetic programs governing uterine morphogenesis and ontogeny of endometrial function in the pig.