title: Altered expression of lysosomal hydrolase, acid α-glucosidase, gene in coronary artery disease.
abstract: BACKGROUND
  Coronary artery disease (CAD) is a common complex disease caused by atherosclerosis. Autophagy is a cellular degradation process that delivers long-lived macromolecules and dysfunctional organelles into lysosomes for digestion. Autophagy regulates lipid and cholesterol metabolism. We have previously shown that expression of autophagic and lysosomal genes is altered in CAD patients. In this study, we investigated gene expression of a lysosomal hydrolase, acid α-glucosidase (GAA), in CAD patients and controls.
  
  
  METHODS
  GAA gene expression was examined in large cohorts of CAD patients (n=248) and ethnically matched controls (n=208). GAA enzymatic activity, protein levels, and transcript levels were determined and compared between CAD patients and controls.
  
  
  RESULTS
  GAA activities in CAD patients were significantly elevated (P<0.05) compared with controls. Consistently, GAA transcription levels were also significantly increased in CAD patients (P<0.01). Multivariate logistic regression analyses (GAA transcript level, hypertension, diabetes, and smoking) revealed that GAA transcript levels were strongly associated with CAD (odds ratio 5.93, 95% confidence interval 2.98-11.78, P=3.89×10(-7)). GAA protein levels were insignificantly increased in CAD patients (P>0.05), likely due to assay insensitivity.
  
  
  CONCLUSIONS
  Compared with controls, GAA gene expression levels in CAD patients were significantly increased, suggesting that GAA may be involved in the CAD development.
authors.affiliation: aCollege of Clinical Medicine, Xinxiang Medical University, Xinxiang, Henan bDivision of Cardiology cShandong Provincial Key Laboratory of Cardiac Disease Diagnosis and Treatment, Affiliated Hospital of Jining Medical University, Jining Medical University, Shandong, China.
authors.forename: Jingyi
authors.initials: J
authors.lastname: Zhang
authors.forename: Ling
authors.initials: L
authors.lastname: Ma
authors.forename: Junping
authors.initials: J
authors.lastname: Zhang
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: Jinguo
authors.initials: J
authors.lastname: Zhang
authors.forename: Bo
authors.initials: B
authors.lastname: Yan
mesh_terms: D000368:Aged; D060050:Angina, Stable / Q000235:genetics / Q000378:metabolism; D000789:Angina, Unstable / Q000235:genetics / Q000378:metabolism; D015153:Blotting, Western; D016022:Case-Control Studies; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000235:genetics* / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics / Q000378:metabolism; D017202:Myocardial Ischemia / Q000235:genetics* / Q000378:metabolism; D016017:Odds Ratio; D012333:RNA, Messenger / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000520:alpha-Glucosidases / Q000235:genetics* / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; C509951:GAA protein, human; D000520:alpha-Glucosidases