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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Pitavastatin Regulates Ang II Induced Proliferation and Migration via IGFBP-5 in VSMC
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Pitavastatin Regulates Ang II Induced Proliferation and Migration via IGFBP-5 in VSMC

机译：匹伐他汀通过VGF通过IGFBP-5调节Ang II诱导的增殖和迁移

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摘要

Angiotensin II (Ang II), a key mediator of hypertensive, causes structural changes in the arteries (vascular remodeling), which involve alterations in cell growth, vascular smooth muscle cell (VSMC) hypertrophy. Ang II promotes fibrotic factor like IGFBP5, which mediates the profibrotic effects of Ang II in the heart and kidneys, lung and so on. The purpose of this study was to identify the signaling pathway of IGFBP5 on cell proliferation and migration of Ang II-stimulated VSMC. We have been interested in Ang II-induced IGFBP5 and were curious to determine whether a Pitavastatin would ameliorate the effects. Herein, we investigated the question of whether Ang II induced the levels of IGFBP5 protein followed by proliferation and migration in VSMC. Pretreatment with the specific Angiotensin receptor type 1 (AT1) inhibitor (Losartan), Angiotensin receptor type 2 (AT2) inhibitor (PD123319), MAPK inhibitor (U0126), ERK1/2 inhibitor (PD98059), P38 inhibitor (SB600125) and PI3K inhibitor (LY294002) resulted in significantly inhibited IGFBP5 production, proliferation, and migration in Ang II-stimulated VSMC. In addition, IGFBP5 knockdown resulted in modulation of Ang II induced proliferation and migration via IGFBP5 induction. In addition, Pitavastatin modulated Ang II induced proliferation and migration in VSMC. Taken together, our results indicated that Ang II induces IGFBP5 through AT1, ERK1/2, P38, and PI3K signaling pathways, which were inhibited by Pitavastatin. These findings may suggest that Pitavastatin has an effect on vascular disease including hypertension.
机译：血管紧张素II（Ang II）是高血压的关键介体，可引起动脉结构变化（血管重塑），涉及细胞生长，血管平滑肌细胞（VSMC）肥大的改变。 Ang II促进像IGFBP5的纤维化因子，介导Ang II在心脏，肾脏，肺等中的纤维化作用。这项研究的目的是确定IGFBP5对Ang II刺激的VSMC细胞增殖和迁移的信号通路。我们对Ang II诱导的IGFBP5感兴趣，并好奇确定匹伐他汀是否可以改善这种作用。在本文中，我们调查了Ang II是否在VSMC中诱导IGFBP5蛋白水平继之以增殖和迁移的问题。使用特定的1型血管紧张素受体（AT1）抑制剂（Losartan），2型血管紧张素受体（AT2）抑制剂（PD123319），MAPK抑制剂（U0126），ERK1 / 2抑制剂（PD98059），P38抑制剂（SB600125）和PI3K抑制剂进行预处理（LY294002）在Ang II刺激的VSMC中导致IGFBP5的产生，增殖和迁移受到显着抑制。另外，IGFBP5敲低导致通过IGFBP5诱导对Ang II诱导的增殖和迁移的调节。另外，匹伐他汀调节的Ang II诱导了VSMC中的增殖和迁移。两者合计，我们的结果表明，Ang II通过AT1，ERK1 / 2，P38和PI3K信号传导途径诱导IGFBP5，而Pitavastatin则抑制了该过程。这些发现可能表明匹伐他汀对包括高血压在内的血管疾病有影响。

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