title: Clinical significance of leukotriene b4 and extracellular matrix metalloproteinase inducer in acute coronary syndrome.
abstract: OBJECTIVE
  Leukotriene B4 (LTB4) and extracellular matrix metalloproteinase (EMMPRIN) have been suggested as modulators of atherosclerotic plaque instability. This study sought to evaluate the potential diagnostic implication of LTB4 and EMMPRIN in patients with acute coronary syndrome (ACS).
  
  
  METHODS
  Patients (n=153) who underwent coronary angiography, including 105 patients diagnosed with ACS, were divided into four groups: stable angina pectoris (SAP, n=19), unstable angina pectoris (UAP, n=39), acute myocardial infarction (AMI, n=66) and control (with normal coronary angiography, n=29). EMMPRIN expression in peripheral blood mononuclear cells was determined by flow cytometry and serum LTB4 levels were measured by ELISA. To examine whether LTB4 can regulate the expression of EMMPRIN and matrix metalloproteinases (MMPs) in macrophages, differentiated THP-1 macrophages were stimulated with different concentrations of LTB4 (10-10-10-7mmol/L). Expression of EMMPRIN was evaluated by Western blotting. MMP-9 mRNA expression and enzymatic activity were determined by RT-PCR and SDS-PAGE gelatin zymography.
  
  
  RESULTS
  Serum LTB4 concentration was significantly higher in AMI and UAP groups, compared with control and SAP groups (p < 0.01). Subgroups analysis showed that LTB4 was significantly higher in the AMI < 24h group, compared with the AMI > 24h group. Expression of EMMPRIN on circulating monocytes was significantly higher in patients with UAP and AMI (> 24h), compared with control, SAP and AMI (< 24h) groups (p < 0.05). In vitro study showed LTB4 up-regulated the expression of EMMPRIN, as well as the expression and activity of MMP-9, in cultured THP-1-derived macrophages (p < 0.05).
  
  
  CONCLUSIONS
  LTB4 and EMMPRIN are associated with the pathogenesis of ACS and may be potential biomarkers for patients with ACS.
authors.affiliation: . richardltung@gmail.com.
authors.forename: Shasha
authors.initials: S
authors.lastname: Xu
authors.forename: Lijiang
authors.initials: L
authors.lastname: Tang
authors.forename: Yafei
authors.initials: Y
authors.lastname: Mi
authors.forename: Jianjun
authors.initials: J
authors.lastname: Jiang
authors.forename: Min
authors.initials: M
authors.lastname: Zhu
authors.forename: Baoguo
authors.initials: B
authors.lastname: Chen
authors.forename: Bin
authors.initials: B
authors.lastname: Wang
authors.forename: Tao
authors.initials: T
authors.lastname: Li
authors.forename: Chenkai
authors.initials: C
authors.lastname: Xu
authors.forename: Jiaochen
authors.initials: J
authors.lastname: Wang
authors.forename: Xianben
authors.initials: X
authors.lastname: Lu
authors.forename: Weili
authors.initials: W
authors.lastname: Ge
authors.forename: Lin
authors.initials: L
authors.lastname: Wang
authors.forename: Jie
authors.initials: J
authors.lastname: Huang
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood*; D000368:Aged; D000369:Aged, 80 and over; D051926:Basigin / Q000097:blood*; D002460:Cell Line; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007975:Leukotriene B4 / Q000097:blood*; D008264:Macrophages / Q000378:metabolism; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000096:biosynthesis; D008875:Middle Aged
chemical_list: C497886:BSG protein, human; D051926:Basigin; D007975:Leukotriene B4; C579270:MMP9 protein, human; D020780:Matrix Metalloproteinase 9