两种“甲状腺特异性”基因的肾表达:促甲状腺激素受体和甲状腺球蛋白。

D F Sellitti, T Akamizu, S Q Doi, G H Kim, J T Kariyil, J J Kopchik, H Koshiyama
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引用次数: 61

摘要

许多肾脏异常伴发甲状腺疾病,其中大多数归因于甲状腺激素对肾脏代谢的影响。在本报告中,我们研究了名义上甲状腺特异性蛋白,促甲状腺激素(TSH)受体(TSHR)和甲状腺球蛋白(Tg)的肾脏表达,作为肾脏和甲状腺功能之间的潜在联系。TSHR的表达已在几种甲状腺外组织中被发现,但其在肾脏中的存在仍有争议。我们使用逆转录酶聚合酶链反应和DNA测序来证明TSHR转录物在人和小鼠肾脏、人肾脏原代培养和绿猴肾脏上皮样细胞系中存在。此外,人肾细胞对TSH的反应是细胞内环磷酸腺苷增加2.5倍,表明存在功能性TSHR蛋白。牛生长激素转基因小鼠进行性肾小球硬化模型与对照小鼠肾脏中TSHR表达的比较表明,转基因动物肾皮质中TSHR转录增加。在体外培养的小鼠系膜细胞中也检测到TSHR转录本,该转录本对TSH有反应,显著增加了三维山赘的形成。聚合酶链反应也证实了Tg转录物在人和小鼠肾脏和小鼠系膜细胞中存在,但TSH或环磷酸腺苷对Tg转录物水平没有影响。单克隆抗tg抗体免疫荧光染色发现系膜细胞细胞质呈阳性染色。这些数据表明肾脏能够表达甲状腺特异性基因TSHR和Tg,这可能介导肾脏甲状腺疾病的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Renal expression of two 'thyroid-specific' genes: thyrotropin receptor and thyroglobulin.

Numerous renal abnormalities accompany thyroid disease, most of which have been ascribed to the effects of thyroid hormone on renal metabolism. In the present report, we investigate the renal expression of the nominally thyroid-specific proteins, thyroid-stimulating hormone (TSH) receptor (TSHR) and thyroglobulin (Tg), as potential links between renal and thyroid function. The expression of TSHR has been identified in several extrathyroidal tissues, but its presence in the kidney remains controversial. We have used reverse-transcriptase polymerase chain reaction and DNA sequencing to demonstrate the presence of TSHR transcript in human and mouse kidney, in a primary culture of human kidney, and in a green monkey kidney epithelioid cell line. Furthermore, human kidney cells responded to TSH with a 2.5- fold increase in intracellular cyclic adenosine monophosphate, suggesting the presence of functional TSHR protein. Comparison of renal expression of TSHR in a bovine growth hormone transgenic mouse model of progressive glomerulosclerosis with control mice suggested increased TSHR transcript in the renal cortex of transgenic animals. TSHR transcript was also detected in mouse mesangial cells in vitro which responded to TSH with significant increases in the formation of three-dimensional hillhocks. Polymerase chain reaction also confirmed the presence of Tg transcript in human and mouse kidneys and in mouse mesangial cells, but no effect of either TSH or cyclic adenosine monophosphate on Tg transcript levels could be discerned. Immunofluorescent staining with a monoclonal anti-Tg antibody identified positive staining in the cytoplasm of mesangial cells. These data suggest that the kidney is capable of expressing the thyroid-specific genes, TSHR and Tg, which could conceivably mediate effects of thyroid disease in the kidney.

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