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首页> 外文期刊>Medicine and science in sports and exercise >Aortic stiffness and aerobic exercise: mechanistic insight from microarray analyses.
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Aortic stiffness and aerobic exercise: mechanistic insight from microarray analyses.

机译：主动脉僵硬和有氧运动：来自微阵列分析的机械洞察力。

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INTRODUCTION/PURPOSE: Regular aerobic exercise reduces aortic stiffness. However, the mechanisms by which chronic exercise lowers arterial stiffness are not known. To determine the molecular mechanisms of these changes, the alteration of gene expression in the aorta by aerobic exercise training was measured with the microarray technique. METHODS/RESULTS: The differences in expression levels of 3800 genes in the abdominal aorta of sedentary control rats (8 wk old) and exercise-trained rats (8 wk old, treadmill running for 4 wk) were compared by the microarray analysis. Aortic pulse wave velocity (PWV) was lower and systemic arterial compliance was higher (both P < 0.05) in the exercise-trained group than in the control group. Of the 323 genes that displayed differential expression (upregulation of 206 genes and downregulation of 117 genes), a total of 29 genes (24 upregulated and 5 downregulated genes) were identified as potential candidate genes that may be involved in vasodilation and arterial destiffening. Using real-time quantitative polymerase chain reaction, we confirmed the results of microarray analysis that prostaglandin EP2 receptor (PGE-EP2R), prostaglandin EP4 receptor (PGE-EP4R), C-type natriuretic peptide (CNP), and endothelial nitric oxide synthase (eNOS) genes were differentially expressed. Furthermore, there were modest correlations between arterial stiffness and levels of these factors. Differential expression of eNOS gene was further verified at protein level by using Western blot analysis. CONCLUSION: These results suggest that exercise training induces the altered expression in several genes including prostaglandin, CNP, and nitric oxide in the aorta and that these molecular changes (particularly eNOS as its protein expression was altered) may contribute, at least in part, to the beneficial effect of exercise training on aortic stiffness.
机译：简介/目的：定期进行有氧运动可降低主动脉僵硬度。但是，长期运动降低动脉僵硬度的机制尚不清楚。为了确定这些变化的分子机制，用微阵列技术测量了有氧运动训练在主动脉中基因表达的改变。方法/结果：通过微阵列分析比较了久坐对照大鼠（8周龄）和运动训练大鼠（8周龄，跑步机运行4周）的腹主动脉中3800个基因的表达水平差异。运动训练组的主动脉脉搏波速度（PWV）较低，全身动脉顺应性较高（均为P <0.05）。在显示差异表达的323个基因（206个基因的上调和117个基因的下调）中，总共29个基因（24个上调和5个下调的基因）被确定为可能参与血管舒张和动脉去硬的潜在候选基因。使用实时定量聚合酶链反应，我们确认了前列腺素EP2受体（PGE-EP2R），前列腺素EP4受体（PGE-EP4R），C型利钠肽（CNP）和内皮型一氧化氮合酶（ eNOS）基因差异表达。此外，在动脉僵硬度和这些因素水平之间存在适度的相关性。通过蛋白质印迹分析，进一步在蛋白质水平上验证了eNOS基因的差异表达。结论：这些结果表明，运动训练可引起主动脉中前列腺素，CNP和一氧化氮等多个基因的表达改变，并且这些分子变化（尤其是其蛋白质表达改变的eNOS）可能至少部分有助于运动训练对主动脉僵硬的有益作用。

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