Özet:
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.
