Laboratory of Cell Biology and Functional Anatomy, Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo 05508-900, Brazil.
Mol Cell Endocrinol. 2013 Jul 15;374(1-2):117-24. doi: 10.1016/j.mce.2013.04.010. Epub 2013 Apr 26.
Hyperthyroidism promotes cardiac hypertrophy and the Angiotensin type 1 receptor (AT1R) has been demonstrated to mediate part of this response. Recent studies have uncovered a potentially important role for the microRNAs (miRNAs) in the control of diverse aspects of cardiac function. Then, the objective of the present study was to investigate the action promoted by hyperthyroidism on β-MHC/miR-208b expression and on α-MHC/miR-208a expression, as well as the possible contribution of the AT1R in this event. The findings of this study confirmed that AT1R is a key mediator of the cardiac hypertrophy induced by hyperthyroidism. Additionally, we demonstrated that like β-MHC, miR-208b was down-regulated in the hyperthyroid group. Similarly, like the expression of its host gene, α-MHC, miR-208a expression was up-regulated in response to hyperthyroidism. Finally, our data suggest for the first time that AT1R mediates the hyperthyroidism-induced increase on cardiac miRNA-208a/α-MHC levels, while does not influence on the reduction of miRNA-208b/β-MHC levels.
甲状腺功能亢进促进心肌肥厚，血管紧张素受体 1（AT1R）已被证明介导了部分反应。最近的研究揭示了 microRNAs（miRNAs）在控制心脏功能的不同方面的潜在重要作用。因此，本研究的目的是研究甲状腺功能亢进对β-MHC/miR-208b 表达和α-MHC/miR-208a 表达的作用，以及 AT1R 在这一事件中的可能贡献。这项研究的结果证实了 AT1R 是甲状腺功能亢进引起的心肌肥厚的关键介质。此外，我们还证明，与β-MHC 一样，miR-208b 在甲状腺功能亢进组中下调。同样，与宿主基因α-MHC 的表达一样，miR-208a 的表达在甲状腺功能亢进时上调。最后，我们的数据首次表明，AT1R 介导甲状腺功能亢进引起的心脏 miRNA-208a/α-MHC 水平的增加，而不影响 miRNA-208b/β-MHC 水平的降低。
