Wang Yuan-Yuan, Li Hui, Wang Xing-Hua, Yuan Meng, Li Guang-Ping
Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Tianjin Institute of Cardiology, Department of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, 300211, People's Republic of China.
J Thromb Thrombolysis. 2016 May;41(4):592-605. doi: 10.1007/s11239-015-1291-6.
This study deciphered the molecular mechanisms of the inhibition of MMP-9 expression using rosuvastatin in cultured human umbilical vein endothelial cells (HUVECs) and apoE knockout mice and whether the combination of rosuvastatin and probucol enhanced this effect. The role that microRNA (miR)-497 plays in the regulation of MMP-9 expression was evaluated in cultured HUVECs and apoE knockout mice using quantitative real-time reverse transcription polymerase chain reaction and Western blotting. First, TNFα significantly increased mitogen-activated protein kinases/extracellular signal-regulated kinase (MAPK/ERK) signaling and MMP-9 levels, and the transfection of miR-497 prevented this increase. The converse results were obtained after miR-497 suppression. Second, the administration of rosuvastatin or the combination of two drugs decreased MAPK/ERK signaling and MMP-9 levels, and the suppression of miR-497 upregulated these levels. Third, the administration of rosuvastatin or the combination of two drugs increased miR-497 expression levels in the aortas of apoE knockout mice, but the levels of serum lipids and plaque areas decreased, which improved plaque components and decreased the MAPK/ERK signaling and MMP-9 levels. Finally, the combination of the two drugs was more effective than the use of rosuvastatin alone. Rosuvastatin inhibits MMP-9 expression by upregulating miR-497 in HUVECs and apoE knockout mice, and the combination of rosuvastatin and probucol enhances this effect.
本研究在培养的人脐静脉内皮细胞(HUVECs)和载脂蛋白E基因敲除小鼠中,解析了瑞舒伐他汀抑制基质金属蛋白酶-9(MMP-9)表达的分子机制,以及瑞舒伐他汀与普罗布考联合使用是否会增强这种作用。使用定量实时逆转录聚合酶链反应和蛋白质印迹法,在培养的HUVECs和载脂蛋白E基因敲除小鼠中评估了微小RNA(miR)-497在MMP-9表达调控中的作用。首先,肿瘤坏死因子α(TNFα)显著增加丝裂原活化蛋白激酶/细胞外信号调节激酶(MAPK/ERK)信号传导和MMP-9水平,而miR-497转染可阻止这种增加。miR-497抑制后得到相反结果。其次,给予瑞舒伐他汀或两种药物联合使用可降低MAPK/ERK信号传导和MMP-9水平,而抑制miR-497可上调这些水平。第三,给予瑞舒伐他汀或两种药物联合使用可增加载脂蛋白E基因敲除小鼠主动脉中miR-497表达水平,但血清脂质水平和斑块面积降低,这改善了斑块成分,并降低了MAPK/ERK信号传导和MMP-9水平。最后,两种药物联合使用比单独使用瑞舒伐他汀更有效。在HUVECs和载脂蛋白E基因敲除小鼠中,瑞舒伐他汀通过上调miR-497抑制MMP-9表达,瑞舒伐他汀与普罗布考联合使用可增强这种作用。