title: Effects of granulocyte-colony stimulating factor on cardiac remodeling after myocardial infarction.
abstract: BACKGROUND
  Recent studies suggest that granulocyte colony-stimulating factor (G-CSF) may be beneficial in the treatment of myocardial infarction (MI). However, the effects of G-CSF on MI are still controversial and the molecular mechanism of G-CSF treatment for repair of the infarcted heart is not fully understood.
  
  
  METHODS
  Mice were divided into three groups: Control, MI and MI treated with G-CSF. Four weeks after MI, we examined cardiac function by Doppler echocardiography and measured non-infarcted myocardial mRNA expression by northern blot analysis.
  
  
  RESULTS
  Cardiac function decreased significantly in the MI groups compared with the sham-operated groups. Additionally, the ratios of E wave to A wave peak velocity (E/A) in the MI groups were higher than in the control group. E/A in G-CSF MI mice was significantly lower than in control MI mice (p<0.01). Matrix metalloproteinase-2 (MMP-2) mRNA expression was significantly increased in the MI groups compared with the control group (p<0.01). Furthermore, mRNA expression in the G-CSF MI group was significantly higher than in the Control MI group (p<0.05).
  
  
  CONCLUSIONS
  G-CSF can prevent the LV remodeling process after MI that accompanies progressive cardiac dysfunction. One of the mechanisms of G-CSF treatment for cardiac remodeling after MI may be overexpression of MMP-2 in non-infarcted myocardium.
authors.affiliation: Department of Internal Medicine and Cardiology, Osaka City University, Graduate School of Medicine, 1-4-3, Asahimachi, Abeno-ku, Osaka 545-8585, Japan. ytakagi@hotmail.co.jp
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Takagi
authors.forename: Minoru
authors.initials: M
authors.lastname: Yoshiyama
authors.forename: Takashi
authors.initials: T
authors.lastname: Omura
authors.forename: Ryo
authors.initials: R
authors.lastname: Matsumoto
authors.forename: Takanori
authors.initials: T
authors.lastname: Kusuyama
authors.forename: Soichiro
authors.initials: S
authors.lastname: Enomoto
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Nakamura
authors.forename: Kaname
authors.initials: K
authors.lastname: Akioka
authors.forename: Kazuhide
authors.initials: K
authors.lastname: Takeuchi
authors.forename: Junichi
authors.initials: J
authors.lastname: Yoshikawa
mesh_terms: D000818:Animals; D015152:Blotting, Northern; D015150:Echocardiography, Doppler; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006352:Heart Ventricles / Q000737:chemistry / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics; D020778:Matrix Metalloproteinase 2 / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000503:physiopathology*; D009206:Myocardium / Q000737:chemistry / Q000473:pathology; D012333:RNA, Messenger / Q000032:analysis; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D012333:RNA, Messenger; D016179:Granulocyte Colony-Stimulating Factor; D020778:Matrix Metalloproteinase 2