title: Potential role for antiangiogenic proteins in the myocardial infarction repair process.
abstract: OBJECTIVE
  Although angiogenic proteins have been identified as positive modulators of myocardial revascularization following acute myocardial infarction, little if anything is known regarding the role that antiangiogenic proteins have in myocardial revascularization. We explored the temporospatial distribution of endothelial-monocyte activating polypeptide (EMAP) II to determine whether antiangiogenic proteins have a role in the repair of myocardial tissue following infarction.
  
  
  METHODS
  A rat model of myocardial infarction was utilized to examine EMAP II distribution (in situ hybridization) and protein expression (Western analysis) over a 6-week period.
  
  
  RESULTS
  At baseline, EMAP II protein and mRNA are minimally expressed with transcription products localizing predominately to the perivascular stroma region in the normal rat myocardium. Six hours following myocardial infarction, EMAP II changes its distribution from the perivascular stroma to an invading inflammatory cell population. This is associated with a 2-fold (P < 0.0009) increase in EMAP II protein and its transcription primarily localized to the infarct region. EMAP II protein expression remains elevated throughout the weeks following the infarction with transcription limited to the infarct region and a notable decrease in EMAP II transcription products noted in the viable vasculature surrounding the infarct zone. Six weeks following myocardial infarction, EMAP II protein is elevated above control, changes its location of transcription from the inflammatory cell population to that of the fibroblasts located in the relative avascular scar tissue, and has resumed its perivascular stromal distribution in the viable periinfarct tissue.
  
  
  CONCLUSIONS
  Thus, the temporospatial distribution of this antiangiogenic protein suggests that negative vascular modulators may have a function in the revascularization process following acute myocardial infarction.
authors.affiliation: Department of Pediatrics, University of Southern California Keck School of Medicine, Los Angeles, California, USA.
authors.forename: Jess L
authors.initials: JL
authors.lastname: Thompson
authors.forename: James A
authors.initials: JA
authors.lastname: Ryan
authors.forename: Mark L
authors.initials: ML
authors.lastname: Barr
authors.forename: Benjamin
authors.initials: B
authors.lastname: Franc
authors.forename: Vaughn A
authors.initials: VA
authors.lastname: Starnes
authors.forename: Margaret A
authors.initials: MA
authors.lastname: Schwarz
mesh_terms: D020533:Angiogenesis Inhibitors / Q000378:metabolism*; D000818:Animals; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D005347:Fibroblasts / Q000378:metabolism; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D009363:Neoplasm Proteins / Q000235:genetics / Q000378:metabolism*; D020286:Pericytes / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D016601:RNA-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014018:Tissue Distribution; D014945:Wound Healing
chemical_list: D020533:Angiogenesis Inhibitors; D016207:Cytokines; D009363:Neoplasm Proteins; D012333:RNA, Messenger; D016601:RNA-Binding Proteins; C077219:small inducible cytokine subfamily E, member 1