title: LAMP-2 gene expression in peripheral leukocytes is increased in patients with coronary artery disease.
abstract: BACKGROUND
  Coronary artery disease (CAD) is a common complex disease that is caused by interaction between genetic and environmental factors. Accumulating evidence indicates that foam cells in the atherosclerotic plaques exhibit the characteristics of lysosomal storage diseases, namely lysosomal accumulation of indigested materials. In patients with lysosomal storage diseases, lysosomal accumulation of lipids and cholesterols in atherosclerotic plaque cells has been observed. However, the roles of lysosomal hydrolases and proteins in the pathogenesis of atherosclerosis and CAD remain unclear.
  
  
  OBJECTIVE
  Lysosomal hydrolases and proteins may be involved in the pathogenesis of atherosclerosis and CAD by affecting lipid and cholesterol metabolism.
  
  
  METHODS
  Expression levels of LAMP-2, a lysosomal membrane marker gene, in the peripheral leukocytes of CAD patients (n = 134) and age- and sex-matched healthy controls (n = 80) were examined at transcription and protein levels with reverse transcriptase-polymerase chain reaction and Western blot analyses, respectively. The results were compared between CAD patients and healthy controls.
  
  
  RESULTS
  LAMP-2 gene expression and LAMP-2 protein levels were significantly increased in the peripheral leukocytes of CAD patients, compared with healthy controls. Furthermore, multivariate logistic regression analyses revealed that CAD is significantly associated with LAMP-2 gene expression levels (odds ratio [OR] 8.84, 95% confidence interval [CI]: 2.15-36.40, P = 0.003) or LAMP-2 protein levels (OR 2.03, 95% CI: 1.15-3.59, P = 0.015).
  
  
  CONCLUSIONS
  In CAD patients, LAMP-2 gene expression in the peripheral leukocytes was significantly increased than were controls, which indicates lysosomal accumulation. These data suggest that insufficient lysosomal hydrolases and proteins may lead to abnormal lipid and cholesterol metabolism, which cause initiation and progression of atherosclerosis and CAD.
authors.affiliation: Shandong Provincial Key Laboratory of Cardiac Disease Diagnosis and Treatment, Division of Cardiac Surgery, Jining Medical College Affiliated Hospital, Jining Medical College, China.
authors.forename: Guanghua
authors.initials: G
authors.lastname: Wu
authors.forename: Jian
authors.initials: J
authors.lastname: Huang
authors.forename: Guanghe
authors.initials: G
authors.lastname: Wei
authors.forename: Lixin
authors.initials: L
authors.lastname: Liu
authors.forename: Shuchao
authors.initials: S
authors.lastname: Pang
authors.forename: Bo
authors.initials: B
authors.lastname: Yan
mesh_terms: D015415:Biomarkers / Q000097:blood; D015153:Blotting, Western; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D002681:China; D003324:Coronary Artery Disease / Q000097:blood* / Q000235:genetics; D006801:Humans; D007962:Leukocytes / Q000737:chemistry*; D016015:Logistic Models; D052119:Lysosomal-Associated Membrane Protein 2; D051907:Lysosomal Membrane Proteins / Q000097:blood* / Q000235:genetics; D016017:Odds Ratio; D012333:RNA, Messenger / Q000097:blood; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; C497811:LAMP2 protein, human; D052119:Lysosomal-Associated Membrane Protein 2; D051907:Lysosomal Membrane Proteins; D012333:RNA, Messenger