title: Neutrophil serine proteases and their endogenous inhibitors in coronary artery ectasia patients.
abstract: OBJECTIVE
  Proteolytic enzymes possibly contribute to coronary artery ectasia (CAE). This study aimed to determine whether neutrophils, neutrophil serine proteases (NSPs), and their endogenous inhibitors participated in the pathological process of CAE.
  
  
  METHODS
  The study consisted of 30 patients with CAE, 30 patients with coronary artery disease (CAD), and 29 subjects with normal coronary arteries (Control). The following circulating items were measured: the main NSPs, including human neutrophil elastase (HNE), cathepsin G (CG), and proteinase 3 (PR3); soluble elastin (sElastin), which was a degradation product of elastin fibres; NSP inhibitors such as α1-protease inhibitor (α1-PI), α2-macroglobulin (α2-MG), secretory leucoprotease inhibitor (SLPI), and elafin; as well as two neutrophil activation markers (myeloperoxidase and lactoferrin) and three classic neutrophil activators [tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), and bacterial endotoxin].
  
  
  RESULTS
  The levels of HNE, CG, and sElastin were elevated in the CAE group. The levels of α1-PI and α2-MG were also significantly increased in the CAE group. The levels of myeloperoxidase and lactoferrin were higher in the CAE group. The levels of TNF-α, IL-8, and endotoxin were unchanged in the CAE group compared with those in the CAD group.
  
  
  CONCLUSIONS
  Neutrophils may participate in the process of vessel extracellular matrix destruction and coronary ectasia by releasing NSPs in a non-classical manner.
authors.affiliation: Cardiac Department, Peking Union Medical College Hospital (PUMCH), Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College; Beijing-China. zhangshuyang103@163.com.
authors.forename: Ruifeng
authors.initials: R
authors.lastname: Liu
authors.forename: Lianfeng
authors.initials: L
authors.lastname: Chen
authors.forename: Wei
authors.initials: W
authors.lastname: Wu
authors.forename: Houzao
authors.initials: H
authors.lastname: Chen
authors.forename: Shuyang
authors.initials: S
authors.lastname: Zhang
mesh_terms: D016022:Case-Control Studies; D056649:Cathepsin G / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood / Q000503:physiopathology*; D003430:Cross-Sectional Studies; D004108:Dilatation, Pathologic / Q000097:blood / Q000503:physiopathology; D004549:Elastin / Q000097:blood; D005260:Female; D005342:Fibrinolysis; D006801:Humans; D019272:Leukocyte Elastase / Q000097:blood; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000201:enzymology*; D057057:Serine Proteases / Q000097:blood
chemical_list: D004549:Elastin; D057057:Serine Proteases; D056649:Cathepsin G; D019272:Leukocyte Elastase