Sex Steroid Hormone Receptors in the Developing Female Reproductive Tract of Laboratory Rodents

Abstract

-Many chemicals released into the environment potentially disrupt the endocrine system in wildlife and humans. Some of these chemicals exhibit estrogenic activity by binding to the estrogen receptors. The developing organism is particularly sensitive to estrogenic chemicals during the critical period in which the induction of long-term changes and persistent molecular alterations in female reproductive tracts occur. Perinatal mouse and rat models can be utilized as indicators for determining the consequences of exposure to exogenous estrogenic agents, including possible xenoestrogens or environmental endocrine disruptors. Estrogen receptors (ER) and estrogen responsive genes, therefore, need to be identified in order to understand the molecular basis of estrogenic actions. Recent identifications of ER subtypes and isoforms make understanding target organ responses to these estrogenic chemicals even more difficult. Indeed, many reports suggest that these chemicals do affect the reproductive and developmental processes of female laboratory rodents that had been perinatally exposed, and that interactions between sex steroid hormone receptors occur. Much information concerning the expression of sex steroid receptors in rodents has been reported concerning the normal development of the Müllerian duct. Thus, accumulated information on the expression of ER subtypes and isoforms as well as that of progesterone and androgen receptors in laboratory rodents is herein reviewed, in addition to the presentation of our own data.

Relaxin (RLX) and estrogen affect estrogen receptor α, vascular endothelial growth factor, and RLX receptor expression in the neonatal porcine uterus and cervix

“…It is well established that patterns of ER expression in FRT tissues are regulated both temporally and spatially during the course of development (Yamashita et al 1989, Glatstein & Yeh 1995, Mowa & Iwanaga 2000, Okada et al 2005. Moreover, aberrant activation of the ER system can have lasting consequences for FRT morphology and function (Miller et al 1998, Markey et al 2005.…”

Pathological study for the effects of in utero and postnatal exposure to diesel exhaust on a rat endometriosis model

“…Alteration of immune system by DE particle exposure may also enhance the pathology of the endometriosis model; however, further investigations are needed to answer the unsolved questions. Moreover, the effect of DE exposure on expression level of sex steroid receptors, which have an important role in development of female reproductive tract (Okada et al, 2005), is a future interest.…”

Immunoendocrine aspects of endometrial function and implantation

“…The binding of the ligand-receptor complex to the hormone response element in the DNA then triggers the transcription of oncogenes and genes encoding growth factors and cytokines. Two subtypes of ESRI, classical ESR1 (ERa) and novel ESR2 (ERb), have been identified in the mouse, rat and human (Okada et al 2005, Saunders 2005). In the uterus, the uterotrophic effects of oestradiol operate through the ESR1 receptor, which has a higher Progesterone-induced blocking factor 1 (C13orf24) has been placed as an 'immune/inflammation modulator', since the structure of the protein is not classically recognised as a growth factor or a cytokine.…”