Expression and role of thyroid-stimulating hormone receptors in proopiomelanocortin-producing pituitary cells

Thyroid ◽  
2020 ◽  
Author(s):  
Rafael Maso Prévide ◽  
Kai Wang ◽  
Kosara Smiljanic ◽  
Marija M Janjic ◽  
Maria Tereza Nunes ◽  
...  
Keyword(s):  
Hormone Receptors ◽  
Thyroid Stimulating Hormone ◽  
Pituitary Cells ◽  
Stimulating Hormone

Auto-Regulation of the Thyroid Gland Beyond Classical Pathways

2020 ◽  
Vol 128 (06/07) ◽  
pp. 437-445 ◽  
Author(s):  
Klaudia Brix ◽  
Joanna Szumska ◽  
Jonas Weber ◽  
Maria Qatato ◽  
Vaishnavi Venugopalan ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Hormone Receptors ◽  
Self Regulation ◽  
Thyroid Stimulating Hormone ◽  
Apical Plasma Membrane ◽  
Deficient Mice ◽  
Stimulating Hormone

AbstractThis mini-review asks how self-regulation of the thyroid gland is realized at the cellular and molecular levels by canonical and non-canonical means. Canonical pathways of thyroid regulation comprise thyroid stimulating hormone-triggered receptor signaling. As part of non-canonical regulation, we hypothesized an interplay between protease-mediated thyroglobulin processing and thyroid hormone release into the circulation by means of thyroid hormone transporters like Mct8. We proposed a sensing mechanism by different thyroid hormone transporters, present in specific subcellular locations of thyroid epithelial cells, selectively monitoring individual steps of thyroglobulin processing, and thus, the cellular thyroid hormone status. Indeed, we found that proteases and thyroid hormone transporters are functionally inter-connected, however, in a counter-intuitive manner fostering self-thyrotoxicity in particular in Mct8- and/or Mct10-deficient mice. Furthermore, the possible role of the G protein-coupled receptor Taar1 is discussed, because we detected Taar1 at cilia of the apical plasma membrane of thyrocytes in vitro and in situ. Eventually, through pheno-typing Taar1-deficient mice, we identified a co-regulatory role of Taar1 and the thyroid stimulating hormone receptors. Recently, we showed that inhibition of thyroglobulin-processing enzymes results in disappearance of cilia from the apical pole of thyrocytes, while Taar1 is re-located to the endoplasmic reticulum. This pathway features a connection between thyrotropin-stimulated secretion of proteases into the thyroid follicle lumen and substrate-mediated self-assisted control of initially peri-cellular thyroglobulin processing, before its reinternalization by endocytosis, followed by extensive endo-lysosomal liberation of thyroid hormones, which are then released from thyroid follicles by means of thyroid hormone transporters.

Effect of peptide nicking in the human chorionic gonadotropin β-subunit on stimulation of recombinant human thyroid-stimulating hormone receptors

1994 ◽  
Vol 130 (1) ◽  
pp. 92-96 ◽  
Author(s):  
Masayoshi Yoshimura ◽  
A Eugene Pekary ◽  
Xuan-Ping Pang ◽  
Loretta Berg ◽  
Laurence A Cole ◽  
...  
Keyword(s):  
Los Angeles ◽  
Chorionic Gonadotropin ◽  
Human Chorionic Gonadotropin ◽  
Hormone Receptors ◽  
Thyroid Stimulating Hormone ◽  
Human Thyroid ◽  
Β Subunit ◽  
Trophoblastic Diseases ◽  
Thyrotropic Activity ◽  
Stimulating Hormone

Yoshimura M, Pekary AE, Pang X-P, Berg L, Cole LA, Kardana A, Hershman JM. Effect of peptide nicking in the human chorionic gonadotropin β-subunit on stimulation of recombinant human thyroid-stimulating hormone receptors. Eur J Endocrinol 1994;130:92–6. ISSN 0804–4643 It is now generally accepted that human chorionic gonadotropin (hCG) has thyroid-stimulating activity. Heterologous forms of the hCG molecule occur in the purified preparations extracted from urine of pregnant women and patients with trophoblastic diseases. This work was undertaken to determine the effect of peptide nicking in the hCG-β subunit on its thyrotropic potency. Using Chinese hamster ovary cells expressing functional human thyroid-stimulating hormone (TSH) receptors, we examined the effect of nicked hCG on cyclic AMP (cAMP) production and receptor binding. The effect of human leukocyte elastase (hLE), a nicking enzyme, on standard hCG also was examined in the cAMP assay and on receptor binding. We studied five hCG preparations extracted from the urine of normal pregnancy (CR-127 and P8) and trophoblastic diseases (C2, C5 and M4). Two preparations (C2, 96% nicked and M4, 100% nicked in the β44–49 region) showed about a 1.5-fold potency of standard hCG CR-127, which is also 20% nicked in the same region. Non-nicked hCG (P8) had the weakest potency among all of the samples tested. Treatment of standard hCG with hLE increased the cAMP response about two-fold. Dose-dependent displacement of bovine [125I]TSH by standard hCG and hLE-digested hCG was observed and was almost identical. We have confirmed the increased in vitro thyrotropic activity of hCG nicked in the β-intercysteine loop on recombinant human TSH receptors. These data suggest that peptide heterogeneity of the hCG molecule may modulate the in vivo thyrotropic activity of hCG in pregnant women and patients with trophoblastic diseases. Jerome M Hershman, Endocrinology-W111D, West Los Angeles VA Medical Center, Los Angeles, California 90073, USA

scholarly journals The Physiological Role of Thyrotropin-Releasing Hormone in the Regulation of Thyroid-Stimulating Hormone and Prolactin Secretion in the Rat

1978 ◽  
Vol 61 (2) ◽  
pp. 441-448 ◽  
Author(s):  
Arthur R. C. Harris ◽  
Dana Christianson ◽  
M. Susan Smith ◽  
Shih-Lieh Fang ◽  
Lewis E. Braverman ◽  
...  
Keyword(s):  
Physiological Role ◽  
Thyroid Stimulating Hormone ◽  
Prolactin Secretion ◽  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Stimulating Hormone

scholarly journals Expression of follistatin mRNA by somatotropes and mammotropes early in the rat estrous cycle.

1993 ◽  
Vol 41 (7) ◽  
pp. 955-960 ◽  
Author(s):  
B L Lee ◽  
G Unabia ◽  
G Childs
Keyword(s):  
Fetal Bovine Serum ◽  
S100 Protein ◽  
Thyroid Stimulating Hormone ◽  
Pituitary Cells ◽  
Folliculostellate Cells ◽  
Complementary Oligonucleotide ◽  
Fetal Bovine ◽  
In Cells ◽  
Stimulating Hormone

We previously found follistatin (FS) mRNA in gonadotropes [predominantly in cells with luteinizing hormone (LH) antigens] and folliculostellate cells (with S100 antigens) in diestrus rats pituitaries. However, earlier in the cycle, when percentages of gonadotropes are lowest, percentages of cells expressing FS are 1.5-2-fold higher than in diestrus. This study was designed to detect FS mRNA and other pituitary antigens to identify the additional cells with dual in situ hybridization and immunolabeling protocols. The mRNA was detected with biotinylated complementary oligonucleotide probes and avidin-biotin-peroxidase complexes. Significant labeling for FS mRNA was found in cells with the following antigens: growth hormone (GH) (7% of pituitary cells); prolactin (PRL) (5%); S100 protein (5%); follicle-stimulating hormone (FSH beta) (4%); LH beta (3%); and thyroid-stimulating hormone (TSH beta) (3%). Optimal conditions for detection included: overnight plating of > 50,000 cells/well (24-well tray) in media containing 10% fetal bovine serum; hybridization at 37 degrees C; and fixation in 2% glutaraldehyde. Whereas FS is expressed predominantly by LH gonadotropes at midcycle, FS mRNA can be expressed by all types of antigen-bearing cells earlier in the cycle. Its function in the pituitary may relate to its role in binding activin, which would result in inhibition of FSH release. However, since activin inhibits secretion of GH, PRL, and adrenocorticotropin (ACTH), FS may also control activin's effects on these cells. The FS-expressing cells may therefore be paracrine or autocrine regulators.

Subclinical Hyperthyroidism: Diagnostic Criteria and Principles of Treatment

2016 ◽  
pp. 75-79
Author(s):  
Vita Galitskaya
Keyword(s):  
Hormone Receptors ◽  
Color Doppler ◽  
Specific Treatment ◽  
Nodular Goiter ◽  
Thyroid Stimulating Hormone ◽  
Free Thyroxine ◽  
Subclinical Hyperthyroidism ◽  
Mineral Density ◽  
Free Triiodothyronine ◽  
Stimulating Hormone

This article presents the European Thyroid Association guidelines for diagnosis and treatment of subclinical hyperthyroidism, 2015. Determination of thyroid1stimulating hormone levels can help to diagnose a variety of pathological conditions: hypertension, cardiac fibrillation, atrial fibrillation, mineral density reduction in bones, menstrual irregularities, infertility, which require specific treatment after detection of hormonal status disorders (subclinical, overt), taking into account the patient’s age. Diagnosis of endogenous subclinical hyperthyroidism is based solely on the results of laboratory tests, not clinical criteria. Endogenous subclinical hyperthyroidism is defined by the presence of sub-normal levels of thyroid-stimulating hormone with normal levels of free thyroxine, total triiodothyronine, and/or free triiodothyronine. There are two categories of endogenous subclinical hyperthyroidism: stage 1 – the level of thyroid-stimulating hormone is 0,1–0,39 mIU/l; stage 2 – the level of thyroid-stimulating hormone is <0.1 mIU/l. The levels of free thyroxine and free triiodothyronine, as a rule, are medium-high value at a subclinical level of thyroid hormone and can help differentiate between endogenous subclinical hyperthyroidism from overt hyperthyroidism. It is recommended to study the thyroid-stimulating hormone level as the first test for the diagnosis of subclinical hyperthyroidism. In identifying low levels of thyroid-stimulating hormone it is necessary to investigate the level of free thyroxine, free or bound triiodothyronine. Patients with primary sub-normal levels of thyroid-stimulating hormone with concentration of thyroid hormones in the upper limit or in normal range should be evaluated within 2-3 months. It is recommended to perform scintigraphy and possible 24-hour test the absorption of radioactive iodine if in patient with 2nd degree endogenous subclinical hyperthyroidism there is nodular goiter to determine treatment strategy. Ultrasonography with color Doppler can be informative for patients with endogenous subclinical hyperthyroidism and nodular goiter. Determining the level of antibodies to thyroid-stimulating hormone receptors can confirm the etiology of autoimmune-induced hyperthyroidism.

Posttraumatic Anterior Hypopituitarism—Revisited: The Role of TRH Provocative Release of Prolactin in the Confirmation of Anterior Pituitary Damage

PEDIATRICS ◽  
1977 ◽  
Vol 59 (6) ◽  
pp. 948-950
Author(s):  
David R. Brown ◽  
J. Michael McMillin
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Thyroid Stimulating Hormone ◽  
Anterior Pituitary Gland ◽  
Serum Prolactin ◽  
Pituitary Insufficiency ◽  
Closed Head Trauma ◽  
One Year ◽  
Stimulating Hormone

We have previously reported a case of anterior pituitary insufficiency in a 14-year-old girl following closed head trauma.1 Endocrine evaluation one year after her accident revealed hypopituitarism manifested by cachexia, hypothyroidism, hypogonadism, and hypoadrenocorticism. Laboratory studies demonstrated deficiencies of adrenocorticotropic hormone, thyroid-stimulating hormone (TSH), growth hormone, and gonadotropic hormones (follicle-stimulating hormone and luteinizing hormone). We postulated that her hypopituitarism was due to anterior pituitary gland destruction rather than stalk section or hypothalamic damage. We have recently measured her serum prolactin concentrations following provocative stimulation with thyrotropin-releasing hormone (TRH), and these results strengthen the evidence for direct anterior pituitary gland destruction and provide a more complete delineation of her endocrinologic function.

Physiological role of galanin in the regulation of anterior pituitary function in humans

1994 ◽  
Vol 266 (1) ◽  
pp. E57-E61 ◽  
Author(s):  
A. Giustina ◽  
M. Licini ◽  
M. Schettino ◽  
M. Doga ◽  
G. Pizzocolo ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Physiological Role ◽  
Thyroid Stimulating Hormone ◽  
Pituitary Function ◽  
Slight Reduction ◽  
Baseline Serum ◽  
Releasing Hormone ◽  
Anterior Pituitary Function ◽  
Stimulating Hormone

The aim of our study was to elucidate the physiological role of the neuropeptide galanin in the regulation of anterior pituitary function in human subjects. Six healthy men (age range 26-35 yr, body mass index range 20-24 kg/m2) underwent in random order 1) an intravenous bolus injection of growth hormone-releasing hormone (GHRH)-(1-29)-NH2 (100 micrograms) + thyrotropin-releasing hormone (TRH, 200 micrograms) + luteinizing hormone-releasing hormone (LHRH, 100 micrograms) + corticotropin-releasing hormone (CRH, 100 micrograms), and 2) intravenous saline (100 ml) at time 0 plus either human galanin (500 micrograms) in saline (100 ml) or saline (100 ml) from -15 to +30 min. Human galanin determined a significant increase in serum GH (GH peak: 11.3 +/- 2.2 micrograms/l) from both baseline and placebo levels. No significant differences were observed between GH values after galanin and those after GHRH alone (24.3 +/- 5.2 micrograms/l). Human galanin significantly enhanced the GH response to GHRH (peak 49.5 +/- 10 micrograms/l) with respect to either GHRH or galanin alone. Human galanin caused a slight decrease in baseline serum adrenocorticotropic hormone (ACTH; 16.3 +/- 2.4 pg/ml) and cortisol levels (8 +/- 1.5 micrograms/dl). Galanin also determined a slight reduction in both the ACTH (peak 27 +/- 8 pg/ml) and cortisol (peak 13.8 +/- 1.3 micrograms/dl) responses to CRH. Baseline and releasing hormone-stimulated secretions of prolactin, thyroid-stimulating hormone, LH, and follicle-stimulating hormone were not altered by galanin. Our data suggest a physiological role for the neuropeptide galanin in the regulation of GH secretion in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

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