Development of radioimmunoassay for bullfrog thyroid-stimulating hormone (TSH): effects of hypothalamic releasing hormones on the release of TSH from the pituitary in vitro

Okada, Reiko; Yamamoto, Kazutoshi; Koda, Aya; Ito, Yoichi; Hayashi, Hiroaki; Tanaka, Shigeyasu; Hanaoka, Yoichi; Kikuyama, Sakaé

doi:10.1016/j.ygcen.2003.09.001

Cited by 57 publications

(28 citation statements)

References 37 publications

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“…In mammals and other higher vertebrates, TRH is the primary regulator of TSH synthesis and secretion, and thus of the thyroid axis. In amphibians, TRH does not regulate thyroid secretion in larvae, but it can stimulate TSH secretion in adults (see Denver 1996, Okada et al 2004. There is now considerable evidence that shows that CRF functions as a larval amphibian TSH releasing factor (reviewed by Denver et al 2002).…”

Section: Discussionmentioning

confidence: 99%

Regulation of pituitary thyrotropin gene expression during Xenopus metamorphosis: negative feedback is functional throughout metamorphosis

Manzon¹,

Denver²

2004

Journal of Endocrinology

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Several hypotheses have been proposed to explain the increase and sustained expression of pituitary thyrotropin (TSH) in the presence of elevated plasma thyroid hormone (TH) concentrations at metamorphic climax in amphibians. It has been proposed that the negative feedback of TH on TSH is inoperative until metamorphic climax, and that it is established at this time by the upregulation of pituitary deiodinase type II (DII); DII converts thyroxine (T 4 ) to 3,5,3 -triiodothyronine (T 3 ). However, earlier investigators, using indirect measures of TSH, reported that TH negative feedback on TSH was functional in premetamorphic tadpoles. In an effort to understand pituitary TSH regulation during amphibian metamorphosis, we analyzed multiple pituitary genes known or hypothesized to be involved in TSH regulation in tadpoles of Xenopus laevis. Tadpole pituitary explant cultures were used to examine direct negative feedback on TSH mRNA expression. Negative feedback is operative in the early prometamorphic tadpole pituitary and both T 3 and T 4 can downregulate TSH mRNA expression throughout metamorphosis. The expression of both DII and TH receptor A mRNAs increased during development and peaked at climax; however, these increases coincided with similar increases in deiodinase type III, which inactivates TH. Moreover, corticotropin-releasing factor (CRF) receptors, CRF binding protein and thyrotropin-releasing hormone receptor type 2 mRNA expression also peaked at climax. Our data suggest that the regulation of TSH is more complex than the timing of DII expression, and likely involves a balance between stimulation of TSH synthesis and secretion by neuropeptides (e.g. CRF) of hypothalamic or pituitary origin, increased pituitary sensitivity to neuropeptides through upregulation of their receptors, and intrapituitary TH levels.

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Section: Discussionmentioning

confidence: 99%

Regulation of pituitary thyrotropin gene expression during Xenopus metamorphosis: negative feedback is functional throughout metamorphosis

Manzon¹,

Denver²

2004

Journal of Endocrinology

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“…The hypothalamic peptide gonadotropin-releasing hormone (GnRH) regulates the biosynthesis and secretion of both gonadotropins; luteinizing hormone (LH) and follicle stimulating hormone (FSH). Besides the well-known function of GnRH in regulating gonadotropins, GnRH treatment has been shown to moderately increase TSH secretion in amphibians (17, 45), suggesting that GnRH can modulate THs at the pituitary level. Several studies have also observed that GnRH can increase thyroxine (3,5,3′,5′- l -tetra-iodothyronine or T4) levels in fish (33, 34) and in amphibians (44, 99).…”

Section: Th Regulation By Gonadotropinsmentioning

confidence: 99%

Crossover of the Hypothalamic Pituitaryâ€“Adrenal/Interrenal, â€“Thyroid, and â€“Gonadal Axes in Testicular Development

2014

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Besides the well-known function of thyroid hormones (THs) for regulating metabolism, it has recently been discovered that THs are also involved in testicular development in mammalian and non-mammalian species. THs, in combination with follicle stimulating hormone, lead to androgen synthesis in Danio rerio, which results in the onset of spermatogenesis in the testis, potentially relating the hypothalamic–pituitary–thyroid (HPT) gland to the hypothalamic–pituitary–gonadal (HPG) axes. Furthermore, studies in non-mammalian species have suggested that by stimulating the thyroid-stimulating hormone (TSH), THs can be induced by corticotropin-releasing hormone. This suggests that the hypothalamic–pituitary–adrenal/interrenal gland (HPA) axis might influence the HPT axis. Additionally, it was shown that hormones pertaining to both HPT and HPA could also influence the HPG endocrine axis. For example, high levels of androgens were observed in the testis in Odonthestes bonariensis during a period of stress-induced sex-determination, which suggests that stress hormones influence the gonadal fate toward masculinization. Thus, this review highlights the hormonal interactions observed between the HPT, HPA, and HPG axes using a comparative approach in order to better understand how these endocrine systems could interact with each other to influence the development of testes.

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“…There are lines of evidence supporting that CRH may function as a TRF in chickens (16), frogs, and teleosts (10,21,23,29,30,32). In chickens, CRH not only induces pituitary ACTH secretion (31) but also stimulates pituitary TSH secretion potently (16).…”

Section: 2 or 4 H) Failed To Stimulate Their Secretion From Cultumentioning

confidence: 99%

“…The dual roles of CRH in chicken pituitary are likely mediated by CRH type I receptor (CRH-R1) and CRH type II receptor (CRH-R2) expressed in corticotrophs and thyrotrophs, respectively (50). In adult frogs, CRH can stimulate TSH secretion and elevate plasma T 4 levels, accompanied by a concurrent release of pituitary ACTH (23,30,33). Moreover, injection of ovine CRH into amphibian larvae is also reported to increase pituitary TSH secretion, elevate plasma thyroid hormone levels, and accelerate tadpole metamorphosis (16,32,(51)(52)(53), a developmental process which involves the morphological and physiological changes orchestrated by thyroid hormone (30,32,53,54).…”

Section: 2 or 4 H) Failed To Stimulate Their Secretion From Cultumentioning

confidence: 99%

“…In contrast, TRH potently induces pituitary GH secretion both in vitro and in vivo, and thus, it is more likely to act as a GH-releasing factor in chickens (3, 14 -20). In amphibians, TRH stimulates pituitary TSH release moderately in adult frogs but not in tadpoles, and it also induces PRL and GH secretion effectively (10,(21)(22)(23). Interestingly, CRH, a well-known ACTH-releasing factor in mammals (24,25), has been demonstrated to act as a TSH-releasing factor (TRF) in chickens, amphibians, and teleosts (16, 21, 26 -30), in addition to its classic action on pituitary ACTH secretion (9,16,29,(31)(32)(33)(34)(35).…”

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confidence: 99%

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Glucagon-Like Peptide (GCGL) Is a Novel Potential TSH-Releasing Factor (TRF) in Chickens: I) Evidence for Its Potent and Specific Action on Stimulating TSH mRNA Expression and Secretion in the Pituitary

Huang

Meng

et al. 2014

Endocrinology

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Our recent study proposed that the novel glucagon-like peptide (GCGL), encoded by a glucagon-like gene identified in chickens and other lower vertebrates, is likely a hypophysiotropic factor in nonmammalian vertebrates. To test this hypothesis, in this study, we investigated the GCGL action on chicken pituitaries. The results showed that: 1) GCGL, but not TRH, potently and specifically stimulates TSH secretion in intact pituitaries incubated in vitro or in cultured pituitary cells monitored by Western blotting or a cell-based luciferase reporter assay; 2) GCGL (0.1nM-10nM) dose dependently induces the mRNA expression of TSHβ but not 5 other hormone genes in cultured pituitary cells examined by quantitative real-time RT-PCR, an action likely mediated by intracellular adenylate cyclase/cAMP/protein kinase A and phospholipase C/inositol 1,4,5-trisphosphate/Ca(2+) signaling pathways coupled to GCGL receptor (GCGLR); 3) GCGLR mRNA is mainly localized in pituitary cephalic lobe demonstrated by in situ hybridization, where TSH-cells reside, further supporting a direct action of GCGL on thyrotrophs. The potent and specific action of GCGL on pituitary TSH expression and secretion, together with the partial accordance shown among the temporal expression profiles of GCGL in the hypothalamus and GCGLR and TSHβ in the pituitary, provides the first collective evidence that hypothalamic GCGL is most likely to be a novel TSH-releasing factor functioning in chickens. The discovery of this novel potential TSH-releasing factor (GCGL) in a nonmammalian vertebrate species, ie, chickens, would facilitate our comprehensive understanding of the hypothalamic control of pituitary-thyroid axis across vertebrates.

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Development of radioimmunoassay for bullfrog thyroid-stimulating hormone (TSH): effects of hypothalamic releasing hormones on the release of TSH from the pituitary in vitro

Cited by 57 publications

References 37 publications

Regulation of pituitary thyrotropin gene expression during Xenopus metamorphosis: negative feedback is functional throughout metamorphosis

Regulation of pituitary thyrotropin gene expression during Xenopus metamorphosis: negative feedback is functional throughout metamorphosis

Crossover of the Hypothalamic Pituitaryâ€“Adrenal/Interrenal, â€“Thyroid, and â€“Gonadal Axes in Testicular Development

Glucagon-Like Peptide (GCGL) Is a Novel Potential TSH-Releasing Factor (TRF) in Chickens: I) Evidence for Its Potent and Specific Action on Stimulating TSH mRNA Expression and Secretion in the Pituitary

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