. 2012 ). The ligand–receptor interaction induces receptor phosphorylation, within seconds, at multiple Ser/Thr sites in the cytoplasmic C-terminal tail by a GPCR kinase. TRH receptors bind to β-arrestin, internalize in clathrin-coated vesicles and
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Patricia Joseph-Bravo, Lorraine Jaimes-Hoy, Rosa-María Uribe, and Jean-Louis Charli
LG Luo and N Yano
Thyrotropin-releasing hormone (TRH), a hypothalamic tripeptide, is expressed in pancreatic islets at peak levels during the late gestation and early neonate period. TRH increases insulin production in cultured beta-cells, suggesting that it might play a role in regulating pancreatic beta-cell function. However, there is limited information on TRH receptor expression in the pancreas. The aim of the present study was to explore the distribution of the TRH receptor in the pancreas and its function in pancreatic beta-cells. TRH receptor type 1 (TRHR1) gene expression was detected by RT-PCR and verified by Northern blotting and immunoblotting in the beta-cell lines, INS-1 and betaTC-6, and the rat pancreatic organ. The absence of TRH receptor type 2 expression in the tissue and cells indicated the tissue specificity of TRH receptor expression in the pancreas. The TRHR1 signals (detected by in situ hybridization) were distributed not only in islets but also in the surrounding areas of the pancreatic ductal and vasal epithelia. The apparent dissociation constant value for the affinity of [(3)H]3-methyl-histidine TRH (MeTRH) is 4.19 in INS-1 and 3.09 nM in betaTC-6. In addition, TRH induced epidermal growth factor (EGF) receptor phosphorylation with a half-maximum concentration of approximately 50 nM, whereas the high affinity analogue of TRH, MeTRH, was 1 nM. This suggested that the affinity of TRH ligands for the TRH receptor influences the activation of EGF receptor phosphorylation in betaTC-6 cells. Our observations suggested that the biological role of TRH in pancreatic beta-cells is via the activation of TRHR1. Further research is required to identify the role of TRHR1 in the pancreas aside from the islets.
Bert De Groef, Sylvia V H Grommen, and Veerle M Darras
secretion ( De Groef et al. 2003 b ). The stimulating effects of TRH on thyrotropes are mediated through the type 1 TRH receptor (TRH-R1) ( De Groef et al. 2003 a ). Changes in the sensitivity of the thyrotropes to the above
Patricia Joseph-Bravo, Lorraine Jaimes-Hoy, and Jean-Louis Charli
localization of TRH endocrine and nonendocrine cell bodies and TRH receptor fields in the hypothalamus and pituitary and of afferents to TRH neurons. TRH-synthesizing neurons in the rat PVN are represented in light purple, the anterior PVN and the mid
Wenxia He, Xiangyan Dai, Xiaowen Chen, Jiangyan He, and Zhan Yin
, the transcriptional levels of other neuropeptide signaling molecules, including Ssts and Sst receptors, Ghrh and Ghrh receptors, Npy receptors, thyrotropin-releasing hormone (Trh) and Trh receptors, corticotrophin-releasing hormone (Crh) and Crh
Sjoerd D Joustra, Onno C Meijer, Charlotte A Heinen, Isabel M Mol, El Houari Laghmani, Rozemarijn M A Sengers, Gabriela Carreno, A S Paul van Trotsenburg, Nienke R Biermasz, Daniel J Bernard, Jan M Wit, Wilma Oostdijk, Ans M M van Pelt, Geert Hamer, and Gerry T M Wagenaar
cell function through paracrine signaling ( Lejeune et al . 1992 ). It is unknown whether TRH receptor ( Trhr1 ) mRNA expression in Leydig cells is decreased in Igsf1 Δ ex1 mice, as occurs in the pituitary of these mice ( Sun et al . 2012 ). Future
Shona Wood and Andrew Loudon
-expressing cells of the PT lack the TRH receptor, therefore cannot be regulated by a conventional hypothalamus peptide (TRH). The PT thyrotrophs are organised with an internal cistern-like structure, perhaps allowing the action of TSH on hypothalamic cells
Stefan Groeneweg, Robin P Peeters, Theo J Visser, and W Edward Visser
biochemical abnormalities in myxedematous patients (Pitt-Rivers 1955, 1956, Trotter 1955 , 1956 ). Later studies showed that TA 3 potently reduces TSH secretion and TRH-receptor expression in mouse thyrotropic pituitary tumor cells ( Gershengorn et al