A comparative study of estrogen receptors α and β in the rat uterus

• Published in: Biology of reproduction Vol. 61; no. 4; pp. 955 - 964
• Main Authors: HONG WANG, MASIRONI, B, ERIKSSON, H, SAHLIN, L
• Format: Journal Article
• Language: English
• Published: Madison, WI Society for the Study of Reproduction 01.10.1999
• Subjects: Animals; Biological and medical sciences; Estradiol - pharmacology; Female; Fundamental and applied biological sciences. Psychology; Hormone metabolism and regulation; Immunohistochemistry; In Situ Hybridization; Mammalian female genital system; Medicin och hälsovetenskap; Ovariectomy; Progesterone - pharmacology; Rats; Rats, Sprague-Dawley; Receptors, Estrogen - chemistry; Uterus - chemistry; Uterus - drug effects; Vertebrates: reproduction; Molecular form; Rat; Rodentia; Estrogen; Gene expression; Ovarian hormone; Vertebrata; Mammalia; Uterus; Female genital system; Sex steroid hormone; Comparative study; Biological receptor
• ISSN: 0006-3363; 1529-7268
• DOI: 10.1095/biolreprod61.4.955

The uterus is an important target organ for steroid hormones. The effects of these hormones are mediated via specific receptors. The aim of this study was to compare the expression, distribution, and regulation of estrogen receptor (ER) alpha and beta in the rat uterus in order to establish possible different biological roles for the two receptor forms. Ovariectomized rats were treated with either estradiol (E(2)), progesterone (P(4)), or combinations of these for 24 or 48 h. The mRNA levels were measured by solution hybridization. Distribution of the mRNAs and receptor proteins was detected by in situ hybridization and immunohistochemistry. The results showed that ERalpha is the dominating subtype in the rat uterus. E(2) seemed to increase the ERalpha mRNA level in the glandular and luminal epithelium, but it caused a decrease of the immunostaining intensity in the glandular epithelium. P(4) reduced ERalpha expression in luminal epithelium whereas no effect was seen in the glandular epithelium. E(2) or P(4) did not alter the expression of ERbeta, on either the mRNA or protein level. In conclusion, the distribution and regulation of ERalpha and ERbeta differ in the different compartments of the rat uterus. The complex uterine responses to E(2) and P(4) are directly or indirectly mediated by differential cell-specific expression of their receptors. The low expression in the uterus and the limited regulation by gonadal steroids in this study suggest that ERbeta probably plays a minor role in the regulation of uterine physiology.