title: Granulocyte-colony stimulating factor directly enhances proliferation of human troponin I-positive cells derived from idiopathic dilated cardiomyopathy through specific receptors.
abstract: BACKGROUND
  Our previous study showed that granulocyte-colony stimulating factor (G-CSF) enhanced bone-marrow-cell migration into the injured heart and that bone-marrow cells differentiated into cardiomyocytes. However, the number of bone-marrow-derived cardiomyocytes seems too small to have a direct, positive impact on pump function. Therefore, we hypothesized that G-CSF directly could affect the host myocardium through G-CSF receptors (G-CSFRs).
  
  
  METHODS
  In experiment 1, we cultured normal mouse heart cells with G-CSF at concentrations of 0, 1, 10, 50, and 100 ng/ml. In experiment 2, we cultured heart cells derived from a recipient with idiopathic cardiomyopathy (IDCM) after heart transplantation. We compared the total number of heart cells and Ki67- and troponin I (TnI)-positive cells with/without G-CSF at 50 ng/ml. We also performed immunochemical staining of the heart specimen from a recipient with IDCM using a rabbit polyclonal anti-G-CSFR antibody.
  
  
  RESULTS
  In experiment 1, mouse heart cells with G-CSF (50 ng/ml) proliferated maximally. In experiment 2, the total numbers of heart cells, Ki67-positive cells. TnI-positive cells, Ki67- and TnI-double-positive cells in the G-CSF group were greater than those in the non-G-CSF group at Days 14 and 28 (p <0.05). In the IDCM heart, G-CSFRs on cardiomyocytes were expressed heterogeneously and widely.
  
  
  CONCLUSIONS
  Granulocyte-colony stimulating factor directly enhanced the proliferation of TnI-positive cells derived from a recipient with IDCM through the G-CSFR.
authors.affiliation: Department of Regenerative Medicine and Tissue Engineering, Osaka, Japan.
authors.forename: Masaki
authors.initials: M
authors.lastname: Hamamoto
authors.forename: Shinji
authors.initials: S
authors.lastname: Tomita
authors.forename: Takeshi
authors.initials: T
authors.lastname: Nakatani
authors.forename: Chikao
authors.initials: C
authors.lastname: Yutani
authors.forename: Seiji
authors.initials: S
authors.lastname: Yamashiro
authors.forename: Taijiro
authors.initials: T
authors.lastname: Sueda
authors.forename: Toshikatsu
authors.initials: T
authors.lastname: Yagihara
authors.forename: Soichiro
authors.initials: S
authors.lastname: Kitamura
mesh_terms: D000328:Adult; D000818:Animals; D002311:Cardiomyopathy, Dilated / Q000473:pathology* / Q000601:surgery; D002455:Cell Division / Q000187:drug effects*; D002478:Cells, Cultured; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology*; D016027:Heart Transplantation; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000032:analysis; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000737:chemistry* / Q000473:pathology*; D016188:Receptors, Granulocyte Colony-Stimulating Factor / Q000032:analysis*; D019210:Troponin I / Q000032:analysis*
chemical_list: D019394:Ki-67 Antigen; D016188:Receptors, Granulocyte Colony-Stimulating Factor; D019210:Troponin I; D016179:Granulocyte Colony-Stimulating Factor