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干扰素γ和碘化物可增强培养的人甲状腺上皮细胞中72kD热休克蛋白的诱导性。

Interferon gamma and iodide increase the inducibility of the 72 kD heat shock protein in cultured human thyroid epithelial cells.

作者信息

Sztankay A, Trieb K, Lucciarini P, Steiner E, Grubeck-Loebenstein B

机构信息

Institute for Biomedical Aging Research of the Austrian Academy of Sciences, Innsbruck.

出版信息

J Autoimmun. 1994 Apr;7(2):219-30. doi: 10.1006/jaut.1994.1017.

Abstract

The 72 kD heat shock protein (hsp 72) has been postulated to play a role in the development of autoimmune disease and has been shown to be overexpressed in the Graves' disease thyroid gland. The expression and modulation of the 72 kD heat shock protein were therefore studied in cultured human thyroid epithelial cells (TEC). TEC from normal thyroid tissue as well as from non-toxic goitres, thyroid adenomas and Graves' disease thyroids were analysed by Western blotting. Potential modulatory effects of heat shock treatment, TSH, IFN gamma, different serum supplements, sodium iodide and sodium selenite were investigated. Hsp 72 was detectable in cells from all tissue types under basal culture conditions and, at increased concentrations, after heat shock treatment. Quantitative evaluation of Western blotting results by densitometer scanning revealed that hsp 72 concentrations were identical in TEC from normal and diseased thyroids. IFN gamma increased the expression of hsp 72 under basal culture conditions as well as after heat shock treatment. TSH had no effect. Sodium iodide did not affect hsp 72 under basal culture conditions, but augmented the susceptibility of TEC to the effect of heat shock treatment. In contrast, sodium selenite had no effect on the expression of hsp 72. These results demonstrate that local as well as environmental factors may facilitate the induction of hsp 72 in TEC. This may be an important factor for the initiation and progression of thyroid autoimmunity. The stimulatory effect of iodide on hsp induction may also provide an explanation for the frequent occurrence of thyroid autoimmune diseases after iodine exposure.

摘要

72kD热休克蛋白(hsp 72)被推测在自身免疫性疾病的发展中起作用,并且已证实在格雷夫斯病甲状腺中过度表达。因此,对培养的人甲状腺上皮细胞(TEC)中72kD热休克蛋白的表达及调节进行了研究。通过蛋白质印迹法分析来自正常甲状腺组织以及非毒性甲状腺肿、甲状腺腺瘤和格雷夫斯病甲状腺的TEC。研究了热休克处理、促甲状腺激素(TSH)、γ干扰素(IFNγ)、不同血清补充剂、碘化钠和亚硒酸钠的潜在调节作用。在基础培养条件下,所有组织类型的细胞中均可检测到hsp 72,热休克处理后其浓度升高。通过光密度计扫描对蛋白质印迹结果进行定量评估显示,正常和患病甲状腺的TEC中hsp 72浓度相同。IFNγ在基础培养条件下以及热休克处理后均增加了hsp 72的表达。TSH无作用。碘化钠在基础培养条件下不影响hsp 72,但增强了TEC对热休克处理作用的敏感性。相反,亚硒酸钠对hsp 72的表达无作用。这些结果表明,局部以及环境因素可能促进TEC中hsp 72的诱导。这可能是甲状腺自身免疫启动和进展的一个重要因素。碘化物对hsp诱导的刺激作用也可能为碘暴露后甲状腺自身免疫疾病的频繁发生提供一种解释。

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