@Article{mcb.2017.014.099,
AUTHOR = {Kefeng  Liu, Zhengyu  Zhang, Ting  Pei, Ziqing  Li, Jingjing  Wang, Hong  Wang, Suning  Ping, Lie  Deng, Linli  Wang, Jintao  Huang, Puyi Sheng, Shuying Liu, Chaohong Li},
TITLE = {Simvastatin Inhibits the Proliferation and Apoptosis of Macrophages Induced by Mechanical and/or Oxidized Low-Density Lipoprotein},
JOURNAL = {Molecular \& Cellular Biomechanics},
VOLUME = {14},
YEAR = {2017},
NUMBER = {2},
PAGES = {101--123},
URL = {http://www.techscience.com/mcb/v14n2/28601},
ISSN = {1556-5300},
ABSTRACT = {This study was designed to investigate the effects of mechanical (MS) and/or oxidized low-density lipoprotein on proliferation and apoptosis of RAW264.7 macrophages and the underlying mechanisms. The cultured quiescent RAW264.7 macrophages were subject to stimulation with MS and/or in the presence or absence of simvastatin and then harvested for Western blot, and immunoflourecence. Either MS or alone could cause increase in cell proliferation and apoptosis, while their combination led to an additive effect. In terms of mechanisms, MS and/or significantly increased phosphorylation levels of MAPKs (ERKs, JNKs and p38MAPK), promoted the reactive oxygen species (ROS) and up-regulated DNA methylation in RAW264.7 macrophages. The increased DNA methylation was associated with proliferation but not apoptosis. In contrast, simvastatin could remarkably inhibit all the effects mentioned above. MS and can simultaneously promote both proliferation and apoptosis of macrophages through activating MAPKs, ROS, and DNA methylation signaling, which can be directly inhibited by the simvastatin treatment. The study results can provide novel information for the pathogenesis and prevention of hypertensive mechanical related vascular diseases.},
DOI = {10.3970/mcb.2017.014.099}
}