Cui Ying, Sun Yin-Wei, Lin Hai-Shuang, Su Wei-Min, Fang Yan, Zhao Ying, Wei Xiao-Qing, Qin Yuan-Hua, Kohama Kazuhiro, Gao Ying
Department of Biochemistry and Molecular Biology, Dalian Medical University, Lvshun, Dalian, 116044, People's Republic of China.
Mol Cell Biochem. 2014 Aug;393(1-2):255-63. doi: 10.1007/s11010-014-2068-5. Epub 2014 May 3.
Matrix metalloproteinases (MMP) play a pivotal role in the pathogenesis of cardiovascular diseases. Their expressions are altered in response to a variety of stimuli, including growth factors, inflammatory markers, and cytokines. In this study, we demonstrated that platelet-derived growth factor-BB (PDGF-BB) induces a dose- and time-dependent increase in MMP-2 expression in rat vascular smooth muscle cells (VSMC). Treatment with either the Rho-associated protein kinase (ROCK) inhibitor Y-27632 or suppression of ROCK-1/2 by small interfering RNA technology significantly reduced the MMP-2 expression, thus suggesting that ROCK regulates such expression. Similar results were observed when VSMC were pretreated with either U0126 or SB203580, which are selective inhibitors of extracellular signal-regulated kinase and p38 mitogen-activated protein kinase, respectively, thus suggesting that these kinases are important for the induction of MMP-2 expression by PDGF-BB. In conclusion, these results described a novel mechanism in atherosclerosis through PDGF-BB signaling in VSMC, in which MMP-2 expression is induced via extracellular signal-regulated kinases and p38 mitogen-activated protein kinase phosphorylation, as well as ROCK.
基质金属蛋白酶(MMP)在心血管疾病的发病机制中起关键作用。它们的表达会因多种刺激而改变,包括生长因子、炎症标志物和细胞因子。在本研究中,我们证明血小板衍生生长因子-BB(PDGF-BB)可诱导大鼠血管平滑肌细胞(VSMC)中MMP-2表达呈剂量和时间依赖性增加。用Rho相关蛋白激酶(ROCK)抑制剂Y-27632处理或通过小干扰RNA技术抑制ROCK-1/2均显著降低了MMP-2表达,因此表明ROCK调节这种表达。当VSMC分别用U0126或SB203580预处理时观察到类似结果,U0126和SB203580分别是细胞外信号调节激酶和p38丝裂原活化蛋白激酶的选择性抑制剂,因此表明这些激酶对于PDGF-BB诱导MMP-2表达很重要。总之,这些结果描述了通过VSMC中PDGF-BB信号传导在动脉粥样硬化中的一种新机制,其中MMP-2表达是通过细胞外信号调节激酶和p38丝裂原活化蛋白激酶磷酸化以及ROCK诱导的。