title: Cyclo-oxygenase-2 (COX-2) expression at the site of recent myocardial infarction: friend or foe?
abstract: BACKGROUND
  Cyclo-oxygenase-2 (COX-2) is induced in cardiomyocytes only in response to stress, such as ischaemia.
  
  
  OBJECTIVE
  To assess COX-2 expression at the site of recent myocardial infarction.
  
  
  METHODS
  COX-2 expression was evaluated by specific immunostaining in cardiomyocytes from 23 subjects who died 10-60 days after acute myocardial infarction. The relation between COX-2 myocardial expression and apoptotic rate was investigated. Cardiomyocyte apoptotic rate was defined as the number of cells co-expressing in situ end labelling of DNA fragmentation (TUNEL) and immunostaining for activated caspase-3.
  
  
  RESULTS
  COX-2 expression was found in cardiomyocytes at the site of infarction in nine of 23 cases (39%). It was associated with fivefold higher apoptotic rates (median 17.9% (interquartile range 11.0-25.4%) v 3.7% (0.6-12.8%); p = 0.016), and apoptotic rate increased progressively from mild to intense COX-2 staining (p for trend 0.009). COX-2 expression co-localised with TUNEL nuclear staining in myocytes, and there was a high concordance between COX-2 and hypoxia induced factor 1-alpha staining (78%, p = 0.021) and between COX-2 and bax (83%, p = 0.014). Subjects showing myocardial COX-2 expression were more likely to have enlarged hearts (p = 0.050), and intense COX-2 staining was strictly associated with symptomatic heart failure (p = 0.035).
  
  
  CONCLUSIONS
  COX-2 is expressed in cardiomyocytes in nearly 40% of cases at the site of recent acute myocardial infarction, even late after the index event. Its expression was associated with extremely high apoptotic rates. These findings suggest a potential cause-effect link between COX-2 expression and enhanced myocardial apoptosis in ischaemic cardiomyopathy.
authors.affiliation: Institute of Cardiology, Catholic University, Rome, Italy. abbatea@yahoo.com
authors.forename: A
authors.initials: A
authors.lastname: Abbate
authors.forename: D
authors.initials: D
authors.lastname: Santini
authors.forename: G G L
authors.initials: GG
authors.lastname: Biondi-Zoccai
authors.forename: S
authors.initials: S
authors.lastname: Scarpa
authors.forename: F
authors.initials: F
authors.lastname: Vasaturo
authors.forename: G
authors.initials: G
authors.lastname: Liuzzo
authors.forename: R
authors.initials: R
authors.lastname: Bussani
authors.forename: F
authors.initials: F
authors.lastname: Silvestri
authors.forename: F
authors.initials: F
authors.lastname: Baldi
authors.forename: F
authors.initials: F
authors.lastname: Crea
authors.forename: L M
authors.initials: LM
authors.lastname: Biasucci
authors.forename: A
authors.initials: A
authors.lastname: Baldi
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D017209:Apoptosis; D015415:Biomarkers / Q000097:blood; D051546:Cyclooxygenase 2; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007527:Isoenzymes / Q000378:metabolism*; D008297:Male; D008565:Membrane Proteins; D009203:Myocardial Infarction / Q000201:enzymology* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000201:enzymology; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D007527:Isoenzymes; D008565:Membrane Proteins; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases