title: Oncostatin-M in myocardial ischemia/reperfusion injury may regulate tissue repair.
abstract: OBJECTIVE
  Oncostatin-M, a member of the gp 130 family of cytokines, has been associated with inflammation, connective tissue production, and extracellular matrix turnover. Since the reperfused heart is associated with an intense inflammatory reaction followed by scar formation, we tested the hypothesis that oncostatin-M is upregulated in response to cardiac injury and may play a part in cardiac repair.
  
  
  METHODS
  Using a canine model of myocardial ischemia/reperfusion injury, we examined the expression of oncostatin-M at various time points of reperfusion, ranging from 1 h to 7 days. In situ hybridization was used to determine oncostatin-M mRNA expression. Immunohistochemistry was performed to detect oncostatin-M protein. Stimulatory effects of oncostatin-M on isolated endothelial cells and fibroblasts were investigated.
  
  
  RESULTS
  Oncostatin-M mRNA expression was detected in ischemic segments within the first 3 h of reperfusion and was persistent over the whole observation period. At the early time points, infiltrating and endothelial cells were the primary source of oncostatin-M mRNA expression. At later time points, macrophages and myofibroblasts were the main contributors. We previously demonstrated in vivo that monocyte-chemoattractant-protein (MCP-1) mRNA is induced early after reperfusion. We stimulated isolated endothelial cells with oncostatin-M and postischemic lymph, which have both upregulated MCP-1 expression in endothelial cells. In addition, isolated fibroblasts stimulated with oncostatin-M demonstrated a dose-dependent proliferative response.
  
  
  CONCLUSIONS
  Oncostatin-M may contribute to the process of healing after myocardial infarction.
authors.affiliation: Department of Cardiology, The Methodist Hospital, Baylor College of Medicine, Houston, Texas, USA. marianne.gwechenberger@akh-wien.ac.at
authors.forename: Marianne
authors.initials: M
authors.lastname: Gwechenberger
authors.forename: Deddo
authors.initials: D
authors.lastname: Moertl
authors.forename: Richard
authors.initials: R
authors.lastname: Pacher
authors.forename: Martin
authors.initials: M
authors.lastname: Huelsmann
mesh_terms: D000818:Animals; D002455:Cell Division; D002478:Cells, Cultured; D004285:Dogs; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D005347:Fibroblasts / Q000378:metabolism; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000473:pathology; D053683:Oncostatin M; D010455:Peptides / Q000378:metabolism*
chemical_list: D010455:Peptides; D053683:Oncostatin M