Kai Zhao1, Xing Sheng Xu, Xiao Meng, Yu Lan Li, Ji Fu Li, Wen Qiang Chen. 1. aDepartment of Cardiology, The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of Shandong University bThe School of Medicine, Shandong University, Jinan, People's Republic of China.
Abstract
OBJECTIVE: The aim of this study was to determine whether autophagy of monocytes attenuates the vulnerability of atherosclerotic plaques. METHODS: The 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. RESULTS: Western 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). CONCLUSION: Autophagy 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.
OBJECTIVE: The aim of this study was to determine whether autophagy of monocytes attenuates the vulnerability of atherosclerotic plaques. METHODS: The 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. RESULTS: Western blot analysis revealed that the expression of beclin-1 and LC3 was significantly lower in acute coronary syndromepatients than in the SAP and control groups (P<0.05). Among the acute coronary syndromepatients, 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). CONCLUSION: Autophagy 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.