Role of corticotropin-releasing hormone as a thyrotropin-releasing factor in non-mammalian vertebrates

Laboratory of Comparative Endocrinology, K.U. Leuven, B3000 Leuven, Belgium.
General and Comparative Endocrinology (Impact Factor: 2.47). 04/2006; 146(1):62-8. DOI: 10.1016/j.ygcen.2005.10.014
Source: PubMed
ABSTRACT
The finding that thyrotropin-releasing hormone does not always act as a thyrotropin (TSH)-releasing factor in non-mammalian vertebrates has led researchers to believe that another hypothalamic factor may exhibit this function. In representatives of all non-mammalian vertebrate classes, corticotropin-releasing hormone (CRH) appears to be a potent stimulator of hypophyseal TSH secretion, and might therefore function as a common regulator of both the thyroidal and adrenal/interrenal axes. CRH exerts its dual hypophysiotropic action through two different types of CRH receptors. Thyrotropes express type 2 CRH receptors, while CRH-induced corticotropin (ACTH) secretion is mediated by type 1 CRH receptors on the corticotropic pituitary cells. The stimulating effect of CRH on both TSH and ACTH release has profound consequences for the peripheral action of both hormonal axes. The simultaneous stimulation of the thyroidal and adrenal/interrenal axes by CRH, possibly fine-tuned by differential regulation of the expression of the different CRH receptor isoforms, provides a potential mechanism for developmental plasticity.
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    • "Thyroid hormone is synthesized and secreted in thyroid gland, and this process is stimulated by Tsh released from pituitary gland. Unlike mammals, Crh rather than Trh is believed to be more potent stimulator of Tsh secretion in fish (De Groef et al., 2006). Therefore, the elevated expressions of crh and tshb genes (Fig. 3B) support increased plasma T4 level. "
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    • "In our study, elevated transcription of the CRH and TSHˇgenesTSHˇgenes were observed in larvae following exposure to 4.30 g/L PM. It has been demonstrated that the production of TSHˇbyTSHˇby the pituitary gland was influenced via negative feedback mechanisms (De Groef et al., 2006; Yu et al., 2011). Increased TSH-serum levels and concomitant reduction in T 4 levels as a compensatory response have been found in rat after oral exposure to 200 or 400 mg/kg PM for 15 days (Wang et al., 2002 ). "
    [Show abstract] [Hide abstract] ABSTRACT: Permethrin (PM), one of the most heavily used synthetic pyrethroids, has the potential to interfere with thyroid hormones in mammals, however, the effect is poorly recognized in aquatic organisms. Herein, embryonic zebrafish were exposed to PM (0, 1, 3 and 10 μg/L) until 72 h post-fertilization. We demonstrated that PM readily accumulated in larvae with a preference for cis-PM, inhibited development and increased thyroxine and 3,5,3′-triiodothyronine levels accompanying increase in the transcription of most target genes, i.e., thyroid-stimulating hormone β, deiodinases, thyroid receptors, involved in the hypothalamic-pituitary-thyroid axis. Further Western blot analysis indicated that transthyretin (TTR) protein was significantly increased. Molecular docking analysis and molecular dynamics simulations revealed that PM fits into three hydrophobic binding pocket of TTR, one of the molecular targets of thyroid hormone disrupting chemicals (THDCs), and forms strong van der Waals interactions with six resides of TTR, including Leu8, Leu 101, Leu125, Thr214, Leu218 and Val229, thus altering TTR activity. Both in vivo and in silico studies clearly disclosed that PM potentially disrupts the thyroid endocrine system in fish. This study provides a rapid and cost-effective approach for identifying THDCs and the underlying mechanisms.
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    • "Since then, CRH-induced TSH release has been found in species of most nonmammalian vertebrate classes (De Groef et al., 2006b) (Fig. 1). At least in frogs and chickens, CRH stimulates the release of ACTH by binding to type 1 CRH receptor (CRHR1) on pituitary corticotropes, while inducing hypophyseal TSH secretion by binding type 2 CRH receptors (CRHR2) on the thyrotropes (De Groef et al., 2003, 2006b Okada et al., 2007). In vivo, CRH-induced ACTH and TSH release would translate to increases in circulating levels of corticosteroids and thyroid hormones, respectively, which was confirmed, using exogenous CRH, in chicken embryos (Meeuwis et al., 1989 ), western spadefoot toad (Spea hammondii) tadpoles (Denver, 1997), and X. laevis larvae (Boorse and Denver, 2004). "
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