Myoblast transplantation for cardiac repair: from automyoblast to allomyoblast transplantation.
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.
Guo
Changfa
C
Department of Cardiac Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Haider
Husnain Kh
HKh
Wang
Chunsheng
C
Tan
Ru-San
RS
Shim
Winston S N
WS
Wong
Philip
P
Sim
Eugene K W
EK
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
D003524:Cyclosporins; D007166:Immunosuppressive Agents