细胞内钙增加在甲状旁腺激素诱导的UMR-106细胞同源脱敏中的作用。

Role of increase in intracellular calcium in PTH-induced homologous desensitization in UMR-106 cells.

作者信息

Ikeda K, Sugimoto T, Fukase M, Fujita T

机构信息

Department of Medicine, Kobe University School of Medicine, Japan.

出版信息

Biochem Biophys Res Commun. 1991 May 15;176(3):1033-6. doi: 10.1016/0006-291x(91)90386-l.

DOI:10.1016/0006-291x(91)90386-l

PMID:1645535

Abstract

Effects of increase in intracellular calcium on PTH-induced homologous desensitization were investigated using calcium ionophores. Pretreatment of UMR-106 cells (rat osteoblast like osteosarcoma cell line) with calcium ionophores (A23187 or ionomycin) for 6h resulted in approximately 50% decrease of PTH-stimulated cAMP production. PTH receptor binding, assessed with 125I-[Nle8,Nle18,Tyr34]PTH-(1-34) as radioligand, was significantly decreased in 10(-6) M calcium ionophore-pretreated (for 6h) cells without affecting the dissociation constant (Kd) for PTH. Minimal effective treatment period was 2h and similar inhibitory effect was observed in 12h-treated cells. These data suggest that increase in intracellular calcium might also act on PTH receptor in the similar manner as protein kinase C activation to induce desensitization.

摘要

使用钙离子载体研究细胞内钙增加对甲状旁腺激素（PTH）诱导的同源脱敏的影响。用钙离子载体（A23187或离子霉素）预处理UMR-106细胞（大鼠成骨样骨肉瘤细胞系）6小时，导致PTH刺激的cAMP产生减少约50%。以125I-[Nle8,Nle18,Tyr34]PTH-(1-34)作为放射性配体评估的PTH受体结合，在10(-6) M钙离子载体预处理（6小时）的细胞中显著降低，而不影响PTH的解离常数（Kd）。最小有效治疗期为2小时，在处理12小时的细胞中观察到类似的抑制作用。这些数据表明，细胞内钙的增加可能也以与蛋白激酶C激活类似的方式作用于PTH受体以诱导脱敏。