Graves' immunoglobulin G stimulates iodide efflux in FRTL-5 thyroid cells.

Graves' immunoglobulin G stimulates iodide efflux in FRTL-5 thyroid cells.
复制标题

DOI:
10.1210/jcem.77.1.8100833
复制
发表时间:
1993-07
期刊:
The Journal of clinical endocrinology and metabolism
影响因子:
--
通讯作者:
Y. Shoda;Y. Kondo;I. Kobayashi
Y. Shoda;Y. Kondo;I. Kobayashi
中科院分区:
其他
文献类型:
--
作者:
Y. Shoda;Y. Kondo;I. Kobayashi

文献摘要

被引文献

相似文献

TSH诱导的FRTL-5细胞(一种来源于正常大鼠甲状腺细胞的细胞系)的I-外排不是由cAMP介导的,而是由细胞内Ca2+信号介导的。已知格雷夫斯患者免疫球蛋白G可以激活甲状腺cAMP通路,但对Ca2+信号的激活知之甚少。我们在此报道,与TSH类似,Graves患者的聚乙二醇沉淀血清部分诱导FRTL-5细胞的I-外排。将在TSH存在下生长的细胞在含1% CS、胰岛素和氢化可的松的Ham’s 10培养基中培养3周。碘化125i预孵育50分钟,标记细胞内碘,血清样品攻毒1分钟。正常混合血清的加入对I-外排几乎没有影响。格雷夫斯免疫球蛋白G组分剂量依赖性地刺激I-外排。12例患者血清相对于合并血清100%的平均效力为217 +/- 56.4%。该数值显著高于8名正常受试者(110 +/- 16.1%)(P < 0.001)。本研究表明Graves甲状腺毒症不仅由腺苷酸环化酶- camp系统介导,而且由磷脂- ca2 +系统介导。
TSH induced I- efflux in FRTL-5 cells, a cell line derived from normal rat thyroid cells, is not mediated by cAMP but intracellular Ca2+ signaling. Graves' patient immunoglobulin G is known to activate the thyroidal cAMP pathway, but little is known about the activation of Ca2+ signaling. We report here that, similarly to TSH, the polyethylenglycol-precipitated serum fraction of Graves' patients induces I- efflux in FRTL-5 cells. The cells grown in the presence of TSH were incubated for 3 weeks in a Ham's 10 medium containing 1% CS, insulin, and hydrocortison for TSH depletion. After preincubating with 125I-iodide for 50 min to label intracellular iodide, the cells were challenged by serum samples for 1 min. The addition of normal pooled-serum hardly affected the I- efflux. The Graves' immunoglobulin G fractions dose-dependently stimulated I- efflux. The averaged potency of 12 patients' sera relative to the values of the pooled serum as 100% was 217 +/- 56.4%. This value was significantly higher (P < 0.001) than that for eight normal subjects (110 +/- 16.1%). The present study is the demonstration suggesting that Graves' thyrotoxicosis is mediated not only by an adenylate cyclase-cAMP system but also by a phospholipid-Ca2+ system.