title: Lower AMP-activated protein kinase level is associated with the vulnerability of coronary atherosclerotic plaques by attenuating the expression of monocyte autophagy.
abstract: BACKGROUND
  Coronary atherosclerotic plaque formation is driven by macrophage infiltration. Monocytes and macrophages contribute to the progression of atherosclerosis. However, research on the relationship between AMP-activated protein kinase (AMPK) and vulnerable atherosclerotic plaques is still insufficient. In the present study, we aimed to elucidate the adaptive mechanism between autophagy of peripheral blood monocytes (PBMs) and the rupture of atherosclerotic plaques. We investigated whether AMPK and autophagy of monocytes can enhance the stability of coronary atherosclerotic plaques in the human body.
  
  
  METHODS
  Samples of PBMs were collected and isolated from all patients with stable angina pectoris (SAP), non-ST-segment elevation acute coronary syndrome, ST-segment elevation acute myocardial infarction, and without coronary artery disease (control). Then, western blot was used to detect the expression levels of AMPK and autophagy-related protein.
  
  
  RESULTS
  The expression levels of beclin-1 and ATG7 were all significantly lower in the acute coronary syndrome groups than those in the SAP and control groups (all P<0.01). The level of phosphorylated AMPK was significantly decreased in patients with acute coronary syndrome compared with those in the SAP and control groups (P<0.01). However, there was no statistical difference between the SAP group and the control group. The activation of mTOR was distinctly increased in the STEMI group (P<0.05).
  
  
  CONCLUSIONS
  Therefore, our work is novel in showing that AMPK of PBMs may decrease plaque vulnerability and subsequent plaque rupture through activation of autophagy.
authors.affiliation: The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, People's Republic of China.
authors.forename: Jing
authors.initials: J
authors.lastname: Cheng
authors.forename: Lei
authors.initials: L
authors.lastname: Qiao
authors.forename: Xingsheng
authors.initials: X
authors.lastname: Xu
authors.forename: Chungang
authors.initials: C
authors.lastname: Zhai
authors.forename: Kai
authors.initials: K
authors.lastname: Zhao
authors.forename: Xiaoping
authors.initials: X
authors.lastname: Ji
authors.forename: Wenqiang
authors.initials: W
authors.lastname: Chen
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism*; D054058:Acute Coronary Syndrome / Q000097:blood / Q000473:pathology*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000787:Angina Pectoris / Q000097:blood / Q000473:pathology*; D051017:Apoptosis Regulatory Proteins / Q000097:blood; D001343:Autophagy; D000071193:Autophagy-Related Protein 7; D000071186:Beclin-1; D015153:Blotting, Western; D003324:Coronary Artery Disease / Q000201:enzymology / Q000473:pathology*; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000097:blood; D008875:Middle Aged; D009000:Monocytes / Q000473:pathology*; D009203:Myocardial Infarction / Q000097:blood / Q000473:pathology*; D044764:Ubiquitin-Activating Enzymes / Q000097:blood
chemical_list: D051017:Apoptosis Regulatory Proteins; C491997:BECN1 protein, human; D000071186:Beclin-1; D008565:Membrane Proteins; D055372:AMP-Activated Protein Kinases; C509349:ATG7 protein, human; D000071193:Autophagy-Related Protein 7; D044764:Ubiquitin-Activating Enzymes