Wu G.,Shandong Provincial Key Laboratory of Cardiac Disease Diagnosis |
Wei G.,Shandong Provincial Key Laboratory of Cardiac Disease Diagnosis |
Wei G.,Jining Medical College Affiliated Hospital |
Huang J.,Shandong Provincial Key Laboratory of Cardiac Disease Diagnosis |
And 4 more authors.
European Journal of Clinical Investigation | Year: 2011
Background Coronary artery disease (CAD) is a common and multifactorial arterial disease that is mainly caused by atherosclerosis. Macrophages, lymphocytes and neutrophils have been implicated in atherosclerotic plaque development. Autophagy, a highly conserved cellular process for the removal of long-lived protein and organelles, plays a variety of pathophysiological roles. However, the roles of autophagy in peripheral leucocytes in atherosclerosis and CAD have not been explored. Materials and methods LC3 is a marker gene for autophagy, and LC3-II, a conjugated form of LC3 protein, is a membrane marker for autophagosome and autophagolysosomes. In this study, LC3 gene expression levels and LC3-II protein levels in peripheral leucocytes were measured in patients with CAD (n=146) and healthy controls (n=87). Results In patients with CAD, LC3 gene expression levels in the peripheral leucocytes were significantly decreased compared with age- and sex-matched healthy controls (P<0·01). LC3-II protein levels were also significantly decreased in patients with CAD (P<0·01). Multivariate logistic analyses showed that decreased LC3 gene expression levels were strongly associated with CAD. There were no differences in LC3 transcripts and LC3-II protein levels between subgroups of patients with CAD. Conclusions LC3 gene expression in the peripheral leucocytes was significantly decreased in patients with CAD, indicating that autophagosome formation is decreased. These data suggest that autophagy in circulating leucocytes may be involved in the pathogenesis of atherosclerosis and CAD. © 2011 The Authors. European Journal of Clinical Investigation © 2011 Stichting European Society for Clinical Investigation Journal Foundation.