4.6 Article

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

期刊

CELLULAR SIGNALLING
卷 25, 期 10, 页码 1949-1954

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2013.06.005

关键词

Thyroid hormone; Tri-iodothyronine; MiR34a; Tubular epithelial cell; Epithelial-to-mesenchymal transition

资金

  1. Natural Science Foundation of Shannxi Province [2011k12-13]
  2. National Science Foundation of China [NSFC 81100080, NSFC 81101396]

向作者/读者索取更多资源

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.

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