Immunodetection of Thyroid Hormone Receptor (Alpha1/Alpha2) in the Rat Uterus and Oviduct

Abstract

Thyroid hormones (THs) play an important role in reproduction and are essential for development in vertebrate species. It has been reported that hypothyroidism in women causes irregular menstruation, frank infertility and difficulty in maintaining pregnancy [10], and hypothyroidism in rodents induces alterations in the estrous cycle and uterine morphology [13]. It has been reported that thyroidectomy causes a decrease in basal plasma levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) [8, 28]. Thyroid hormone receptors (THR) mediate the cellular response to thyroid hormone (T3) by regulating target gene transcription. THR are the products of two different genes, erbAá and erbAâ. The mammalian erbAá gene produces two mRNAs, erbAá1 (alpha1) and erbAá2 (alpha2). Alpha1 codes for the alpha-thyroid hormone receptor (TRá1), whereas alpha2 codes for an orphan nuclear receptor (TRá2) which does not bind T3. TRá2 competes with TRá1 and TRâ for specific DNA binding sites, thereby antagonizing T3 action. Because the erbAá gene produces both a transcriptional activator (TRá1) and its specific inhibitor (TRá2), regulation of the alternative processing of alpha1 and alpha2 mRNA may provide an important mechanism for determining the cellular response to THs [12]. In the present study, we have immunohistochemically investigated the existence and localization of THR (alpha1/ alpha2) in rat uterus and oviduct.