Anti-TSHR Antibody (M22) is a selective agonist targeting TSHR (thyroid-stimulating hormone receptor), acting through competitive binding to the extracellular domain of TSHR. Anti-TSHR Antibody (M22) can mimic the biological effects of thyroid-stimulating hormone (TSH), activating downstream cAMP-PKA and other signaling pathways. Anti-TSHR Antibody (M22) can stimulate the proliferation of thyroid follicular epithelial cells and human umbilical vein endothelial cells (HUVECs), promote angiogenesis and tube formation, cell migration, and also upregulate the expression of angiogenesis-related proteins such as PROX1. Anti-TSHR Antibody (M22) can be used in research areas such as the mechanisms of goiter formation in Graves' disease (GD), angiogenesis regulation, and TSHR antagonist screening [1] [2] [3].
In Vivo, In female BALB/c mice, pretreatment with L-T3 (5 μg/d, i.p., for 4 consecutive days) to suppress endogenous TSH effects, followed by treatment with Anti-TSHR Antibody (M22) (0.5 μg; intraperitoneal injection; single dose; measured 24 hours after administration), significantly increases serum free T4 (FT4) levels and the mRNA expression levels of sodium-iodide symporter (NIS) and thyroid peroxidase (TPO) in thyroid tissue[2].
In Vitro, Anti-TSHR Antibody (M22) (0.125-8 μg/mL; 24-72 h) promotes the proliferation of human thyroid follicular epithelial cells (Nthy-ori 3-1) and human umbilical vein endothelial cells (HUVECs) in a dose- and time-dependent manner[1]. Anti-TSHR Antibody (M22) (0.125, 0.5 μg/mL; 4-12 h) promotes the tube formation ability of HUVECs in a dose-dependent manner, with improvements in parameters such as total branch length and mesh area[1]. Anti-TSHR Antibody (M22) (0.5 μg/mL; 12 h) significantly promotes the migration of HUVECs[1]. Anti-TSHR Antibody (M22) (0, 0.5 μg/mL; 72 h) induces the significant upregulation of 16 proteins and the significant downregulation of 24 proteins in HUVECs, among which PROX1 protein, closely related to angiogenesis, which is the most significantly upregulated[1].
References:
[1]. Yuan Y, et al. Proangiogenic effect of thyrotropin receptor stimulating antibody in human umbilical vein endothelial cells. Endocrine. 2025 Feb;87(2):697-706.
[2]. Neumann S, et al. A selective TSH receptor antagonist inhibits stimulation of thyroid function in female mice. Endocrinology. 2014 Jan;155(1):310-4.
[3]. Liu Y, et al. Expression of functional thyroid-stimulating hormone receptor in microglia[C]//Annales d'Endocrinologie. Elsevier Masson, 2022, 83(1): 40-45.
In Vivo, In female BALB/c mice, pretreatment with L-T3 (5 μg/d, i.p., for 4 consecutive days) to suppress endogenous TSH effects, followed by treatment with Anti-TSHR Antibody (M22) (0.5 μg; intraperitoneal injection; single dose; measured 24 hours after administration), significantly increases serum free T4 (FT4) levels and the mRNA expression levels of sodium-iodide symporter (NIS) and thyroid peroxidase (TPO) in thyroid tissue[2].
In Vitro, Anti-TSHR Antibody (M22) (0.125-8 μg/mL; 24-72 h) promotes the proliferation of human thyroid follicular epithelial cells (Nthy-ori 3-1) and human umbilical vein endothelial cells (HUVECs) in a dose- and time-dependent manner[1]. Anti-TSHR Antibody (M22) (0.125, 0.5 μg/mL; 4-12 h) promotes the tube formation ability of HUVECs in a dose-dependent manner, with improvements in parameters such as total branch length and mesh area[1]. Anti-TSHR Antibody (M22) (0.5 μg/mL; 12 h) significantly promotes the migration of HUVECs[1]. Anti-TSHR Antibody (M22) (0, 0.5 μg/mL; 72 h) induces the significant upregulation of 16 proteins and the significant downregulation of 24 proteins in HUVECs, among which PROX1 protein, closely related to angiogenesis, which is the most significantly upregulated[1].
References:
[1]. Yuan Y, et al. Proangiogenic effect of thyrotropin receptor stimulating antibody in human umbilical vein endothelial cells. Endocrine. 2025 Feb;87(2):697-706.
[2]. Neumann S, et al. A selective TSH receptor antagonist inhibits stimulation of thyroid function in female mice. Endocrinology. 2014 Jan;155(1):310-4.
[3]. Liu Y, et al. Expression of functional thyroid-stimulating hormone receptor in microglia[C]//Annales d'Endocrinologie. Elsevier Masson, 2022, 83(1): 40-45.