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Aruldhas, Mariajoseph Michael
- An Update on Human Thyroid Hormone Receptors in Health and Disease: Chemistry, Physiology and Pathophysiology
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1 Department of Endocrinology, Dr. ALM Post-Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Taramani-Velachery Link Road, Chennai – 600113, IN
1 Department of Endocrinology, Dr. ALM Post-Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Taramani-Velachery Link Road, Chennai – 600113, IN
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Journal of Endocrinology and Reproduction, Vol 17, No 1 (2013), Pagination: 57-78Abstract
Iodothyronines, the tetra- and tri-iodothyronines (T4 and T3), commonly known as thyroid hormones (THs), are secreted by thyroid glands. Thyroid hormones influence the growth and differentiation of every organ of the body via specific nuclear receptors (TRs), which belong to the nuclear receptor superfamily. Though thyroid glands secrete predominantly T4 (which remains bound to its serum binding proteins), T3 is the biologically active TH. Free T4 enters the target cells through specific transporters and is converted into T3 by cell-specific isoforms of cytoplasmic 5' deiodinase, which regulate the circulating T3 levels and its availability for nuclear TRs in a tissue-specific manner. T3 is then translocated to the nucleus, with the help of NADPH-dependent cytosolic transporter, where it binds to the monomers of TR subtypes (TRα and TRβ). Prior to the binding of T3, TR monomer dimerizes with the 9-cis retinoic acid or retinoid X receptor (RXR) and the TR-RXR heterodimer, in association with corepressors, binds to specific TR response element (TRE) in the target genes. Upon T3 binding to the TR monomer of the TR-RXR-TRE complex, corepressors get released paving way for the binding of coactivators, thereby inducing the transcription of T3-responsive genes. Apart from the canonical nuclear signalling mechanism, membrane-mediated signalling by THs occurs through its interaction with plasma membrane integrin ανβ3. The impact of TH status and TR signalling on a broad range of genes makes studying its effect in vivo a difficult task. Studies on knock-in/out/mutant animal models and humans harboring several mutations of TR isoforms have helped explain various disorders of TH action, particularly the hypothyroid condition associated with the resistance to TH action. The aim of this review is to provide the readers with the information on THs biosynthesis along with the recent progress in TR signalling and its physiological impact on human health.Keywords
Hormone Resistance, HPT Axis, Nuclear receptors, TRα/β, Thyroglobulin.
- Molecular Mechanism Underlying the Temporal Shift in Androgen Action in Post-Natal Rat Epididymis Due to Gestational-Onset Hypothyroidism
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1 Bungtown Road, Cold Spring Harbor Laboratories, Cold Spring Harbor, New York, 11724, US
2 Department of Biomedical and Diagnostic Sciences, UT College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996-4550, US
3 Texas Tech University Health Sciences Centre, 5001 El Paso Dr, Texas, US
4 Department of Endocrinology, Dr.ALM Post Graduate Institute of Basic Medical Sciences,University of Madras-Taramani Campus, Chennai-600 113, IN
1 Bungtown Road, Cold Spring Harbor Laboratories, Cold Spring Harbor, New York, 11724, US
2 Department of Biomedical and Diagnostic Sciences, UT College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996-4550, US
3 Texas Tech University Health Sciences Centre, 5001 El Paso Dr, Texas, US
4 Department of Endocrinology, Dr.ALM Post Graduate Institute of Basic Medical Sciences,University of Madras-Taramani Campus, Chennai-600 113, IN
Source
Journal of Endocrinology and Reproduction, Vol 20, No 1 (2016), Pagination: 66-75Abstract
Thyroid hormones are important regulators of male fertility and mammalian testis with has specific T3 receptors has emerged as its target. Men with history of congenital or juvenile onset hypothyroidism suffer infertility. The epididymis plays a pivotal role in post-testicular maturation of sperm. Recently we reported that transient gestational–onset hypothyroidism leads to infertility in the progeny of rats by affecting sperm maturation due to decreased androgen receptor (Ar) status in the epididymis. In the present study we tested the hypothesis “transient gestational exposure to antithyroid drugs during critical periods of differentiation of male reproductive tract organs may interfere with the functions of epididymis in F1 progeny by modifying the expression of Ar gene, and activity of its protein and the key steroidogenic enzyme, 5α-reductase”. To test the hypothesis, pregnant rats were exposed to the antithyroid drug methimazole (0.05% through drinking water) from embryonic day (ED)9 to 14/18/21covering specific periods of testicular and other male reproductive tract organs differentiation to induce hypothyroidism. Male pups with transient gestational hypothyroidism showed subnormal levels of serum testosterone, and estradiol, along with decreased expression of Ar, and 5α-reductase activity in the epididymis of pre-puberal rats at postnatal day (PND)29, whereas there was normal/boosted Ar expression, and 5α-reductase activity peripubertal rat epididymis at PND 49. Taken together, the present study and our previous report point out that gestational-onset hypothyroidism affect fertility of F1 progeny through an age-dependent divergent effect on 5α-reductase activity and AR gene expression in the epididymis.Keywords
Androgen Receptor, Dihydrotestosterone, 5α-Reductase, Testosterone, Thyroid Hormone.References
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