Growth and function of well differentiated FRTL-5 thyroid cells depend on thyrotropin as its main regulatory hormone. We demonstrate here that stable transfection of FRTL-5 cells with the human thyrotropin receptor cDNA results in cellular transformation of these cells with altered cell shape and loss of contact inhibition. The transformed cells replicate in soft agar and form invasive tumors when cell suspensions are implanted onto nude mice. They have lost their thyrotropin dependent growth and their ability to concentrate iodide and synthesize thyroglobulin. But they still express the rat thyrotropin receptor mRNA and accumulate cAMP in response to thyrotropin stimulation. However, although the full length human thyrotropin receptor cDNA is integrated into their genome, transformed cells do not express the human thyrotropin receptor mRNA.
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http://dx.doi.org/10.1016/0006-291x(92)91631-y | DOI Listing |
J Appl Toxicol
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Changjiang Basin Ecology and Environment Monitoring and Scientific Research Center, Changjiang Basin Ecology and Environment Administration, Ministry of Ecology and Environment, Wuhan, China.
Fluoxetine (FLX), a typical selective serotonin reuptake inhibitors, has been frequently detected in aquatic environment and wild fish. However, little is known about its effect on thyroid endocrine system. In the present study, zebrafish (Danio rerio) embryos were exposed to 1, 3, 10, and 30 μg/L of FLX for 6 days.
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Nephrology, Yokohama Municipal Citizen's Hospital, Yokohama, JPN.
Hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHI) is a novel class of orally administered medications for renal anemia in patients with end-stage renal disease (ESRD). Roxadustat, a HIF-PHI, has a structure similar to that of triiodothyronine and may work as an agonist for thyroid hormone receptor-beta in the pituitary gland and/or hypothalamus. Therefore, roxadustat may cause central hypothyroidism due to suppressing thyroid-stimulating hormone (TSH) release in the pituitary gland and/or thyrotropin-releasing hormone release in the hypothalamus.
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October 2024
School of Medicine and Health Sciences Atma Jaya Catholic University of Indonesia - St Carolus Hospital, Jakarta, Indonesia.
Numerous thyroid diseases can impact patients' lives, one of which is Graves' ophthalmopathy (GO). Graves' ophthalmopathy is a progressive thyroid-related disease that causes eye symptoms due to an autoimmune reaction targeting thyrotropin/thyroid stimulating hormone (TSH) receptors in the orbital space. This condition can be easily recognized by the patient, including exophthalmos, pain, swelling, double vision, and impaired vision.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg 194223, Russia.
The approaches to correct thyroid deficiency include replacement therapy with thyroid hormones (THs), but such therapy causes a number of side effects. A possible alternative is thyroid-stimulating hormone (TSH) receptor activators, including allosteric agonists. The aim of this work was to study the effect of ethyl-2-(4-(4-(5-amino-6-(-butylcarbamoyl)-2-(methylthio)thieno[2,3-d]pyrimidin-4-yl)phenyl)--1,2,3-triazol-1-yl) acetate (TPY3m), a TSH receptor allosteric agonist developed by us, on basal and thyroliberin (TRH)-stimulated TH levels and the hypothalamic-pituitary-thyroid (HPT) axis in male rats with high-fat diet/low-dose streptozotocin-induced type 2 diabetes mellitus (T2DM).
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January 2025
I.M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, Russia.
Graves' disease is caused by overactivation of the thyroid-stimulating hormone receptor (TSHR). One approach for its treatment may be the use of negative allosteric modulators (NAM) of TSHR, which normalize TSHR activity and do not cause thyroid hormone (TH) deficiency. The aim of the work was to study the effect of a new compound 5-amino-4-(4-bromophenyl)-2-(methylthio)thieno[2,3-d]pyrimidine-6-carboxylic acid N-tert-butylamide (TPY4) on the basal and TSH-stimulated TH production in cultured FRTL-5 thyrocytes and on basal and thyrotropin-releasing hormone (TRH)-stimulated TH levels in the blood of rats.
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