标题：Autophagy of monocytes attenuates the vulnerability of coronary atherosclerotic plaques
作者：Zhao, Kai; Xu, Xing Sheng; Meng, Xiao; Li, Yu Lan; Li, Ji Fu; Chen, Wen Qiang
作者机构：[Zhao, Kai; Xu, Xing Sheng; Meng, Xiao; Li, Ji Fu; Chen, Wen Qiang] Shandong Univ, Qilu Hosp, Key Lab Cardiovasc Remodeling & Funct Res, Chinese Minis 更多
通讯作者地址：[Chen, WQ]Shandong Univ, Qilu Hosp, Key Lab Cardiovasc Remodeling & Funct Res, Chinese Minist Educ,Dept Cardiol, 107 Wen Hua Xi Rd, Jinan 250012, Shan 更多
来源：CORONARY ARTERY DISEASE
关键词：atherosclerosis; autophagy; beclin-1; light chain 3; vulnerable plaques
摘要：ObjectiveThe aim of this study was to determine whether autophagy of monocytes attenuates the vulnerability of atherosclerotic plaques.MethodsThe study group comprised 50 patients with stable angina pectoris (SAP), 50 patients with unstable angina pectoris (UAP), 40 patients with acute myocardial infarction (AMI), and 30 patients without coronary artery disease (control). Peripheral blood monocytes (PBMs) were isolated and the expression levels of the proteins beclin-1 and light chain 3 (LC3) (autophagy-specific proteins) in the PBMs were analyzed by western blot. A laser scanning confocal microscope was used to determine the levels of LC3 in the PBMs.ResultsWestern blot analysis revealed that the expression of beclin-1 and LC3 was significantly lower in acute coronary syndrome patients than in the SAP and control groups (P<0.05). Among the acute coronary syndrome patients, the expression level of beclin-1 and LC3 in the AMI group was significantly decreased compared with that in the UAP group (P<0.05). However, there was no statistical difference between the SAP group and the control group. The results of immunofluorescence assays showed that the fluorescence intensity of LC3 in the PBMs of AMI patients was significantly lower than that in those of UAP patients (P<0.05), which was also significantly decreased compared with that in those of SAP patients and the control group (P<0.05). Expression levels of beclin 1 in the UAP and AMI groups had a negative linear correlation with C-reactive protein levels (r=-0.531, P<0.05; r=-0.589, P<0.05, respectively).ConclusionAutophagy of PBMs is involved in the pathogenesis of plaque vulnerability and subsequent plaque rupture. Enhancing the autophagy of PBMs may be a new therapeutic target for stabilizing atherosclerotic plaques.