Angiotensin II regulates microRNA-132/-212 in hypertensive rats and humans.

Angiotensin II regulates microRNA-132/-212 in hypertensive rats and humans.
复制标题

DOI:
10.3390/ijms140611190
复制
发表时间:
2013-05-27
影响因子:
5.6
通讯作者:
Sheikh SP
Sheikh SP
中科院分区:
生物学2区
文献类型:
--
作者:
Eskildsen TV;Jeppesen PL;Schneider M;Nossent AY;Sandberg MB;Hansen PB;Jensen CH;Hansen ML;Marcussen N;Rasmussen LM;Bie P;Andersen DC;Sheikh SP

文献摘要

参考文献

被引文献

相似文献

microRNAs(miRNAs)是一类能够对多种靶mRNA的翻译进行微调的非编码小分子RNA,是心血管发育和疾病的重要调控因子。miRNAs参与了心肌肥厚、心力衰竭和心肌梗死后的重塑;然而,miRNAs参与高血压的研究尚未彻底。我们最近报道了特定的miRNAs在血管紧张素II受体(AT 1 R)信号传导中起着不可或缺的作用,特别是在Gαq信号通路激活后。由于AT 1 R阻断剂被广泛用于治疗高血压,我们采用miRNA微阵列和qPCR分析,对大鼠和高血压患者中血管紧张素II(AngII)介导的高血压的潜在miRNA进行了详细分析。在慢性AngII输注后,高血压(159 ± 12 mm Hg)和心脏肥大大鼠的心脏、主动脉壁和肾脏中miR-132和miR-212高度增加。此外,内皮素受体(另一种Gαq偶联受体)的激活也增加了miR-132和miR-212。我们试图通过推理AT 1 R阻断剂可能减少miR-132和miR-212来扩展这些观察结果。我们分析了冠状动脉搭桥术后剩余动脉组织中的乳腺动脉组织样本。事实上,我们发现接受AT 1 R阻断剂治疗的旁路手术患者的人动脉中miR-132和miR-212的表达水平降低,而β-阻断剂治疗没有影响。综上所述,这些数据表明miR-132和miR-212参与AngII诱导的高血压,为高血压疾病机制提供了新的视角。
MicroRNAs (miRNAs), a group of small non-coding RNAs that fine tune translation of multiple target mRNAs, are emerging as key regulators in cardiovascular development and disease. MiRNAs are involved in cardiac hypertrophy, heart failure and remodeling following cardiac infarction; however, miRNAs involved in hypertension have not been thoroughly investigated. We have recently reported that specific miRNAs play an integral role in Angiotensin II receptor (AT1R) signaling, especially after activation of the Gαq signaling pathway. Since AT1R blockers are widely used to treat hypertension, we undertook a detailed analysis of potential miRNAs involved in Angiotensin II (AngII) mediated hypertension in rats and hypertensive patients, using miRNA microarray and qPCR analysis. The miR-132 and miR-212 are highly increased in the heart, aortic wall and kidney of rats with hypertension (159 ± 12 mm Hg) and cardiac hypertrophy following chronic AngII infusion. In addition, activation of the endothelin receptor, another Gαq coupled receptor, also increased miR-132 and miR-212. We sought to extend these observations using human samples by reasoning that AT1R blockers may decrease miR-132 and miR-212. We analyzed tissue samples of mammary artery obtained from surplus arterial tissue after coronary bypass operations. Indeed, we found a decrease in expression levels of miR-132 and miR-212 in human arteries from bypass-operated patients treated with AT1R blockers, whereas treatment with β-blockers had no effect. Taken together, these data suggest that miR-132 and miR-212 are involved in AngII induced hypertension, providing a new perspective in hypertensive disease mechanisms.
DOI: 10.1007/s11906-011-0235-6
发表时间: 2012-02-01
影响因子: 5.6
作者:
Batkai, Sandor;Thum, Thomas
通讯作者: Thum, Thomas
DOI: 10.1161/circresaha.111.251546
发表时间: 2011-09-30
影响因子: 20.1
作者:
Katare R;Riu F;Mitchell K;Gubernator M;Campagnolo P;Cui Y;Fortunato O;Avolio E;Cesselli D;Beltrami AP;Angelini G;Emanueli C;Madeddu P
通讯作者: Madeddu P
DOI: 10.1016/j.yexcr.2010.04.002
发表时间: 2010-06-10
影响因子: 3.7
作者:
Andersen, Ditte C.;Jensen, Charlotte H.;Sheikh, Soren P.
通讯作者: Sheikh, Soren P.
DOI: 10.1002/stem.72
发表时间: 2009-01-01
期刊: STEM CELLS
影响因子: 5.2
作者:
Andersen, Ditte Caroline;Andersen, Peter;Sheikh, Soren Paludan
通讯作者: Sheikh, Soren Paludan
DOI: 10.2147/jep.s28907
发表时间: 2012
影响因子: --
作者:
Roberts RE
通讯作者: Roberts RE