mProX™ Human TSHR Stable Cell Line

Gulbins A, et al. "Potential involvement of the bone marrow in experimental Graves' disease and ." Frontiers in endocrinology, 2023.
Graves' disease, an autoimmune disorder affecting the thyroid, is caused by auto-antibodies targeting the thyroid stimulating hormone receptor (TSHR). This stimulation results in hyperthyroidism and the most common extra-thyroidal manifestation, thyroid eye disease (TED). In this study, the researchers investigated the potential role of bone marrow activation in the development of Graves' disease and TED, and whether interfering with insulin-like growth factor 1 receptor (IGF-1R) signaling could prevent this activation. Results showed that immunization with TSHR led to an increase in certain immune cells, which was prevented by treatment with an IGF-1R antagonist. Additionally, TSHR immunization resulted in increased expression of pro-inflammatory molecules in the bone marrow, which was also blocked by IGF-1R blockade. Furthermore, linsitinib, the IGF-1R antagonist, induced an upregulation of arginase-1, a regulator of immune responses, leading to reduced levels of arginine in the bone marrow and inhibition of immune cells. These findings indicate that linsitinib-mediated immune-inhibition may be a potential treatment for Graves' disease and TED.
Pubmed: 37810891   DOI: 10.3389/fendo.2023.1252727

Liang C, et al. "Thyrotropin receptor autoantibody (TRAb) enhance the expression of thyrotropin ." Cellular and molecular biology (Noisy-le-Grand, France), 2023.
The documented expression of thyrotropin receptor (TSHR) in non-thyroid tissue has raised interest in investigating its presence in medulla oblongata regions, specifically in cases of hyperthyroidism-associated encephalopathy. This research aimed to explore the expression of functional TSHR in cerebral vascular endothelial cells of mice with Graves' disease (GD) as well as the impact of thyrotropin receptor autoantibody (TRAb) on this expression. Through various techniques including RT-qPCR, Western blot, and immunofluorescence, the location and expression of the TSHR gene and protein were determined in vivo. Additionally, the effect of TRAb on functional TSHR expression was studied in vitro using bEnd.3 cells. The findings revealed that medulla oblongata vascular endothelial cells from GD mice displayed elevated TSHR levels compared to control mice. In an in vitro experiment, it was discovered that treatment with a monoclonal TSHR-specific agonistic antibody (M22) led to an increase in TSHR expression at both the protein and mRNA levels. Furthermore, the production of cAMP was notably higher in bEnd.3 cells treated with M22 compared to those treated with IBMX alone. These results suggest that TSHR is not only expressed but also functionally active in the medulla oblongata of mice and in vitro-cultured bEnd.3 cells. Moreover, TRAb (M22) was found to enhance TSHR expression on bEnd.3 cells.
Pubmed: 37807332   DOI: 10.14715/cmb/2023.69.9.10