Thyroid hormone inhibits TGFβ1 induced renal tubular epithelial to mesenchymal transition by increasing miR34a expression

被引:28
作者
Lu, Xiaozhao [1 ]
Chen, Ziqiang [2 ]
Liang, Hongliang [3 ]
Li, Zhaohui [1 ]
Zou, Xiaorong [1 ]
Luo, Huiwen [1 ]
Guo, Wangang [4 ]
Xu, Lijuan [1 ]
机构
[1] 323 Hosp PLA, Dept Nephrol, Xian 710054, Peoples R China
[2] Second Mil Med Univ, Changhai Hosp, Dept Orthopaed Surg, Shanghai 200433, Peoples R China
[3] Fourth Mil Med Univ, Dept Cardiovasc Surg, Xijing Hosp, Xian 710032, Peoples R China
[4] Fourth Mil Med Univ, Dept Cardiol, Tangdu Hosp, Xian 710038, Peoples R China
基金
美国国家科学基金会;
关键词
Thyroid hormone; Tri-iodothyronine; MiR34a; Tubular epithelial cell; Epithelial-to-mesenchymal transition; DIABETIC-NEPHROPATHY; SUBCLINICAL HYPOTHYROIDISM; DOWN-REGULATION; KIDNEY-DISEASE; PATHWAYS; FIBROSIS; GROWTH; MODEL;
D O I
10.1016/j.cellsig.2013.06.005
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
The interactions between kidney and thyroid functions have been known for many years, but how the thyroid affects the kidney function is largely unknown. Here we analyzed the role of T3 on the tubular epithelial-to-mesenchymal transition (EMT), which is recognized to play pivotal roles in the process of renal fibrosis. T3 was found to significantly inhibit the TGF beta 1 induced EMT in human proximal tubular epithelial cell line HK-2. Meanwhile, T3 induced the expression of miR34a. Molecularly, the T3 receptor could directly bind the T3R recognition motif at the -1505 to -1526 bp and -604 to -609 bp regions in the miR34a promoter and transcriptionally activate the expression of miR34a upon T3 treatment. Inhibition of the miR34a by miR34a knockdown nearly blocked the effects of T3 on EMT. Taken together, our study here revealed that thyroid hormone T3 could inhibit TGF beta 1 induced renal tubular epithelial to mesenchymal transition by increasing miR34a expression. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:1949 / 1954
页数:6
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