title: Autophagy in atherosclerosis: a phenomenon found in human carotid atherosclerotic plaques.
abstract: BACKGROUND
  Autophagy has been found to be involved in animal and cell models of atherosclerosis, but to date, it lacks general observation in human atherosclerotic plaques. Here, we investigated autophagy in smooth muscle cells (SMCs), endothelial cells (ECs), and macrophages in human atherosclerotic plaques via transmission electron microscopy (TEM), western blotting, and immunohistochemistry analysis.
  
  
  METHODS
  The histopathologic morphology of these plaques was observed via hematoxylin and eosin staining. The ultrastructural morphology of the SMCs, ECs, and macrophages in these plaques was observed via TEM. The localization of microtubule-associated protein 1 light chain 3 (MAP1-LC3), a relatively special maker of autophagy, in plaques was observed by double fluorescent immunochemistry and western blotting.
  
  
  RESULTS
  All of these human atherosclerotic plaques were considered advanced and unstable in histologically observation. By double fluorescent immunochemistry, the expression of LC3-II increased in the SMCs of the fibrous cap, the macrophages, and the microvascular ECs of the plaque shoulders. The protein level of LC3-II by western blotting significantly increased in plaques compared with normal controls. In addition, TEM observation of plaques revealed certain features of autophagy in SMCs, ECs, and macrophages including the formation of myelin figures, vacuolization, and the accumulation of inclusions in the cytosol. These results indicate that autophagy is activated in SMCs, ECs, and macrophages in human advanced atherosclerotic plaques.
  
  
  CONCLUSIONS
  Our study is to demonstrate the existence of autophagy in human atherosclerotic plaques by different methods, which may contribute to the development of pharmacological approaches to stabilize vulnerable and rupture-prone lesions.
authors.forename: Huihui
authors.initials: H
authors.lastname: Liu
authors.forename: Yongjun
authors.initials: Y
authors.lastname: Cao
authors.forename: Tong
authors.initials: T
authors.lastname: Tong
authors.forename: Jijun
authors.initials: J
authors.lastname: Shi
authors.forename: Yanlin
authors.initials: Y
authors.lastname: Zhang
authors.forename: Yaping
authors.initials: Y
authors.lastname: Yang
authors.affiliation: Department of Neurology, Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004; Institute of Neuroscience, Soochow University, Suzhou, Jiangsu 215123, China.
authors.forename: Chunfeng
authors.initials: C
authors.lastname: Liu
mesh_terms: D050197:Atherosclerosis / Q000378:metabolism / Q000503:physiopathology*; D001343:Autophagy / Q000502:physiology*; D042783:Endothelial Cells / Q000473:pathology; D006801:Humans; D066298:In Vitro Techniques; D046529:Microscopy, Electron, Transmission; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000473:pathology; D058226:Plaque, Atherosclerotic / Q000378:metabolism / Q000503:physiopathology* / Q000648:ultrastructure
chemical_list: C477012:MAP1LC3A protein, human; D008869:Microtubule-Associated Proteins