Elevated mechanical stress applied to vascular walls is well known to modulate vascular remodeling and plays a part in the pathogenesis of atherosclerosis. On the other hand, docosahexaenoic acid (DHA), an n-3 polyunsaturated fatty acid, has been shown to protect against several types of cardiovascular diseases including atherosclerosis and hypertension. The aim of this study was to clarify the effect of pulsatile pressure stress and DHA on angiotensin II-induced proliferation and migration in A7r5 vascular smooth muscle cells (VSMCs). Pulsatile pressure of between 80 and 160 mmHg was repeatedly applied to VSMCs at a frequency of 4 cycles per min using an apparatus that we developed. Cell proliferation and migration were evaluated using a live cell movie analyzer. Application of pulsatile pressure stress for 24 h significantly increased cell proliferation. Angiotensin II also significantly increased cell proliferation in the presence or absence of pressure stress. DHA significantly inhibited angiotensin II-induced cell proliferation regardless of the pressure load. Angiotensin II significantly induced cell migration regardless of the pulsatile pressure load. Pulsatile pressure stress alone slightly, but not significantly, induced cell migration. DHA inhibited angiotensin II-induced VSMC proliferation and migration under abnormal pressure conditions. Pressure stress tended to induce extracellular signal-regulated kinase (ERK) phosphorylation in the absence of angiotensin II, whereas it significantly induced ERK phosphorylation in the presence of angiotensin II. However, the pressure-induced ERK phosphorylation was not observed in the DHA-treated VSMCs. Our findings may contribute to the understanding of the beneficial effect of DHA on various cardiovascular disorders.

中文翻译：

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二十二碳六烯酸在脉动压力下抑制血管紧张素II诱导的A7r5血管平滑肌细胞增殖和迁移。

众所周知，施加于血管壁的机械应力升高会调节血管重构，并在动脉粥样硬化的发病机理中起作用。另一方面，二十二碳六烯酸（DHA）是一种n-3多不饱和脂肪酸，已被证明可预防多种类型的心血管疾病，包括动脉粥样硬化和高血压。这项研究的目的是阐明脉压压力和DHA对血管紧张素II诱导的A7r5血管平滑肌细胞（VSMC）增殖和迁移的影响。使用我们开发的设备，以每分钟4个周期的频率将80至160 mmHg的脉动压力重复施加到VSMC。使用活细胞电影分析仪评估细胞增殖和迁移。施加脉动压力应激24小时可显着增加细胞增殖。在存在或不存在压力应激的情况下，血管紧张素II也显着增加细胞增殖。无论压力负荷如何，DHA均能显着抑制血管紧张素II诱导的细胞增殖。血管紧张素II显着诱导细胞迁移，而不管脉动压力负荷如何。单独的脉搏压力仅轻微但不显着诱导细胞迁移。DHA在异常压力条件下抑制血管紧张素II诱导的VSMC增殖和迁移。在不存在血管紧张素II的情况下，压力应激倾向于诱导细胞外信号调节激酶（ERK）磷酸化，而在存在血管紧张素II的情况下，压力应激则明显诱导ERK磷酸化。然而，在DHA处理的VSMC中未观察到压力诱导的ERK磷酸化。我们的发现可能有助于理解DHA对各种心血管疾病的有益作用。