Critical role of exogenous nitric oxide in ROCK activity in vascular smooth muscle cells.
Critical role of exogenous nitric oxide in ROCK activity in vascular smooth muscle cells.
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DOI：
10.1371/journal.pone.0109017
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Higashi Y
中科院分区：
文献类型：
--
作者：
Maruhashi T;Noma K;Iwamoto Y;Iwamoto A;Oda N;Kajikawa M;Matsumoto T;Hidaka T;Kihara Y;Chayama K;Nakashima A;Goto C;Liao JK;Higashi Y
Rho相关激酶（ROCK）信号通路介导细胞增殖、迁移、黏附、凋亡和收缩等多种细胞功能，参与动脉粥样硬化的发病机制。内源性一氧化氮（NO）具有抗动脉粥样硬化的作用，而外源性NO介导的心血管作用仍存在争议。本研究旨在观察外源性NO对血管平滑肌细胞（VSMCs）ROCK活性的影响。采用改良的Boyden小室法检测血管平滑肌细胞迁移。ROCK活性通过Western印迹分析在小鼠和人VSMC和用或不用血管紧张素II（Ang II）和/或硝普钠（SNP）（NO供体）处理的小鼠的主动脉中测量。与SNP的共同治疗抑制了Ang II诱导的细胞迁移和ROCK活性在小鼠和人VSMC中的增加。类似地，皮下注射SNP基本上抑制了小鼠主动脉输注Ang II 2周后ROCK活性的增加。这些结果表明，在体外和体内给予外源性NO可以抑制VSMCs的ROCK活性。
Rho-associated kinase (ROCK) signaling pathway has been shown to mediate various cellular functions including cell proliferation, migration, adhesion, apoptosis, and contraction, all of which may be involved in pathogenesis of atherosclerosis. Endogenous nitric oxide (NO) is well known to have an anti-atherosclerotic effect, whereas the exogenous NO-mediated cardiovascular effect still remains controversial. The purpose of this study was to evaluate the effect of exogenous NO on ROCK activity in vascular smooth muscle cells (VSMCs) in vitro and in vivo. VSMCs migration was evaluated using a modified Boyden chamber assay. ROCK activities were measured by Western blot analysis in murine and human VSMCs and aorta of mice treated with or without angiotensin II (Ang II) and/or sodium nitroprusside (SNP), an NO donor. Co-treatment with SNP inhibited the Ang II-induced cell migration and increases in ROCK activity in murine and human VSMCs. Similarly, the increased ROCK activity 2 weeks after Ang II infusion in the mouse aorta was substantially inhibited by subcutaneous injection of SNP. These findings suggest that administration of exogenous NO can inhibit ROCK activity in VSMCs in vitro and in vivo.
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