
Expression and Role of Thyrotropin Receptors in Proopiomelanocortin-Producing Pituitary Cells
Author(s) -
Rafael Maso Prévide,
Kai Wang,
Kosara Smiljanić,
Marija M. Janjic,
Maria Tereza Nunes,
Stanko S. Stojilković
Publication year - 2021
Publication title -
thyroid
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.918
H-Index - 142
eISSN - 1557-9077
pISSN - 1050-7256
DOI - 10.1089/thy.2020.0222
Subject(s) - corticotropic cell , proopiomelanocortin , thyrotropic cell , medicine , endocrinology , anterior pituitary , pituitary gland , receptor , gonadotropic cell , thyrotropin releasing hormone receptor , biology , immunocytochemistry , somatotropic cell , chemistry , hormone , hormone receptor , cancer , breast cancer
Background: Thyrotropin (TSH) is well known as the hormone of the anterior pituitary thyrotrophs responsible for acting in the thyroid gland, where it stimulates synthesis and release of thyroid hormones through G s and G q/11 protein coupled TSH receptors (TSHRs). Methods: In this study, we examined whether the functional TSHRs are also expressed in cultured rat pituitary cells, using double immunocytochemistry, quantitative reverse transcription-polymerase chain reaction analysis, cAMP and hormone measurements, and single-cell calcium imaging. Results: Double immunocytochemistry revealed the expression of TSHRs in cultured corticotrophs and melanotrophs, in addition to previously identified receptors in folliculostellate cells. The functional coupling of these receptors to the G q/11 signaling pathway was not observed, as demonstrated by the lack of TSH activation of IP 3 -dependent calcium mobilization in these cells when bathed in calcium-deficient medium. However, TSH increased cAMP production in a time- and concentration-dependent manner and facilitated calcium influx in single corticotrophs and melanotrophs, indicating their coupling to the G s signaling pathway. Consistent with these findings, TSH stimulated adrenocorticotropin and β-endorphin release in male and female pituitary cells in a time- and concentration-dependent manner without affecting the expression of proopiomelanocortin gene. Conclusions: These results indicate that TSH is a potential paracrine modulator of anterior pituitary corticotrophs and melanotrophs, controlling the exocytotic but not the transcriptional pathway in a cAMP/calcium influx-dependent manner.