| Co-Investigator(Kenkyū-buntansha) |
SATOH Hiroshi Niigata University, Medical and Dental Hospital, Professor, 医歯学総合病院, 教授 (10125768)
NAKAZAWA Mikio Niigata University, Faculty of Medicine, Professor, 医学部, 教授 (80143759)
TOYO-OKA Teruhiko Tokyo University Hospital, Faculty of Medicine, Professor, 医学部, 教授 (00146151)
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| Research Abstract |
The prognosis of patients with dilated eardiomyopathy(DCM) is still poor and cardiac transplantation is the most life-saving treatment in the advances cases. Cell transplantation is currently gaining evidence as a potential means of improving the prognosis of patients with heart failure. To treat DCM, we transplanted normal skeletal myoblast(SkM), to TO-2 strain hamsters, a representative model of human hereditary DCM, of which δ-sarcoglycan(SG) gene is deleted. We confirmed no rejection between TO-2 and golden hamsters by interchanging skin graft in the pilot study. SkM were isolated from the limbs of 3 weeks old normal golden hamsters. We transplanted SkM leveled to 5 weeks old TO-2 hearts. 4',6-Diamidino-2-phenylindole, dihydrochloride(DAPI) was used for nucleus staining, and 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate(DiI) was used for cell membrane staining. At 5 weeks after SkM transplantation, fast skeletal muscle type of skeletal muscle myosin heavy chain(fast-MHC) was detected by Western blotting analysis. DAPI and DiI positive cells were clearly detected in the left ventricle in the grafted TO-2. δ-SG, fast-and slow-MHC were immunologically stained in the grafted TO-2 hearts, but not in the control TO-2 hearts. Moreover, connexin-43 was expressed on the interface of cells that expressed δ-SG. These results suggest that SkM were successfully allografted to DCM hamster. These methods would provide a new strategy for the treatment of DCM.
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