title: Myoblast transplantation for cardiac repair: from automyoblast to allomyoblast transplantation.
abstract: BACKGROUND
  We sought to compare host immune cell kinetics, survival profile of donor skeletal myoblasts, and skeletal myoblast graft efficacy after autologous and allogeneic skeletal myoblast transplantation into a rat model of myocardial infarction.
  
  
  METHODS
  One week after myocardial infarction, 128 animals were divided into four groups: group 1 (n = 24, receiving medium only), group 2 (n = 24, receiving medium and cyclosporine), group 3 (n = 40, autologous skeletal myoblast transplantation), and group 4 (n = 40, allogeneic skeletal myoblast transplantation with cyclosporine treatment). Rats were euthanized 10 minutes, 1 day, and 4, 7, and 28 days later. Host immune cell kinetics were assessed by immunohistochemical studies for macrophages, and CD4+ and CD8+ lymphocytes. Donor skeletal myoblast survival was confirmed by tracking prelabeled signals, and quantified by beta-gal assay. Heart function was evaluated by echocardiography.
  
  
  RESULTS
  A transient immune cell infiltration was demonstrated in group 3, with macrophage infiltration on day 1 and day 4, CD8+ cell infiltration on day 4 and day 7, and CD4+ cell infiltration on day 4. In group 4, immunocyte infiltration was slightly more severe than that in group 3. Automyoblasts and allomyoblasts showed no significant difference of survival from day 1 to day 7 (p > 0.10); however, on day 28, automyoblasts showed better survival than allomyoblasts (p < 0.05). Transplantation of allomyoblasts increased systolic heart function and limited heart dilation after myocardial injury to a similar degree as automyoblasts (p > 0.10).
  
  
  CONCLUSIONS
  The use of allomyoblasts is feasible and effective for cardiac repair with immunosuppressive treatment as compared with automyoblasts.
authors.affiliation: Department of Cardiac Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
authors.forename: Changfa
authors.initials: C
authors.lastname: Guo
authors.forename: Husnain Kh
authors.initials: HKh
authors.lastname: Haider
authors.forename: Chunsheng
authors.initials: C
authors.lastname: Wang
authors.forename: Ru-San
authors.initials: RS
authors.lastname: Tan
authors.forename: Winston S N
authors.initials: WS
authors.lastname: Shim
authors.forename: Philip
authors.initials: P
authors.lastname: Wong
authors.forename: Eugene K W
authors.initials: EK
authors.lastname: Sim
mesh_terms: D000818:Animals; D017690:Cell Transplantation / Q000379:methods*; D003524:Cyclosporins / Q000494:pharmacology*; D004195:Disease Models, Animal; D005260:Female; D006084:Graft Rejection; D006085:Graft Survival; D007150:Immunohistochemistry; D007166:Immunosuppressive Agents / Q000494:pharmacology; D008297:Male; D032448:Myoblasts, Skeletal / Q000276:immunology / Q000637:transplantation*; D009203:Myocardial Infarction / Q000473:pathology / Q000601:surgery*; D011336:Probability; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012038:Regeneration / Q000502:physiology; D012307:Risk Factors; D012680:Sensitivity and Specificity; D014182:Transplantation, Autologous; D014184:Transplantation, Homologous; D020257:Ventricular Remodeling / Q000502:physiology
chemical_list: D003524:Cyclosporins; D007166:Immunosuppressive Agents