Fathi Mohammad, Gharakhanlou Reza, Rezaei Razieh
Department of Physical Education and Sport Sciences, Faculty of Humanities Sciences, Lorestan University, Khorramabad, Iran Electronic Address:
Department of Physical Education and Sport Sciences, Faculty of Humanities Sciences, Tarbiyat Modares University, Tehran, Iran.
Cell J. 2020 Jul;22(Suppl 1):133-140. doi: 10.22074/cellj.2020.7014. Epub 2020 Jul 18.
MicroRNAs (miRNAs) play a key role in the development of the heart. Recent studies have shown that miR- 1 and miR-133 are key regulators of cardiac hypertrophy. Therefore, we aimed to evaluate the effect of an endurance training (ET) program on the expressions of these miRNAs and their transcriptional network.
In this experimental study, cardiac hypertrophy was induced by 14 weeks of ET for 1 hour per day, 6 days per week at 75% VO2 max). The rats (221 ± 23 g) in the experimental (n=7) and control (n=7) groups were anesthetized to evaluate heart morphology changes by echocardiography. Next, we evaluated expressions of miR-1 and miR-133, and heart and neural crest derivatives express 2 , , histone deacetylase 4 (Hdac4) and serum response factor () gene expressions by real-time polymerase chain reaction (PCR). Finally, the collected data were evaluated by the independent t test to determine differences between the groups.
The echocardiography result confirmed physiological hypertrophy in the experimental group that underwent ET as shown by the increased left ventricular weight/body surface area (LVW/BSA) (P=0.004), LVW/body weight (BW) (P=0.011), left ventricular diameter end-diastolic (LVDd) (P=0.003), and improvements in heart functional indexes such as fractional shortness (FS) (P=0.036) and stroke volume (SV) (P=0.002). There were significant increases in the expressions of miR-1 (P=0.001) and miR-133 (P=0.004). The expressions of , and genes significantly increased (P<0.001) in the experimental group Compared with the control group. The expression of did not significantly change.
The expressions of miR-1 and miR-133 and their target genes appeared to be involved in physiological hypertrophy induced by ET in these rats.
微小RNA(miRNA)在心脏发育中起关键作用。近期研究表明,miR-1和miR-133是心肌肥大的关键调节因子。因此,我们旨在评估耐力训练(ET)计划对这些miRNA及其转录网络表达的影响。
在本实验研究中,通过每天1小时、每周6天、持续14周的ET(最大摄氧量的75%)诱导心肌肥大。对实验(n=7)组和对照组(n=7)的大鼠(221±23 g)进行麻醉,通过超声心动图评估心脏形态变化。接下来,我们通过实时聚合酶链反应(PCR)评估miR-1和miR-133的表达,以及心脏和神经嵴衍生物表达2、组蛋白去乙酰化酶4(Hdac4)和血清反应因子()基因的表达。最后,通过独立t检验评估收集的数据,以确定组间差异。
超声心动图结果证实,接受ET的实验组出现生理性肥大,表现为左心室重量/体表面积(LVW/BSA)增加(P=0.004)、LVW/体重(BW)增加(P=0.011)、左心室舒张末期直径(LVDd)增加(P=0.003),以及心脏功能指标如缩短分数(FS)(P=0.036)和每搏输出量(SV)(P=0.002)得到改善。miR-1(P=0.001)和miR-133(P=0.004)的表达显著增加。与对照组相比,实验组中、和基因的表达显著增加(P<0.001)。的表达没有显著变化。
miR-1和miR-133及其靶基因的表达似乎参与了ET诱导的这些大鼠的生理性肥大。