| Aim Various etiologies may cause inreversible injury to cardiac cells, which were replaced by fibroblasts to form scar tissue successively because cardiomyocytes lack the ability of regeneration after birth. Quantitative deficiency of cardiac musles and progressive ventricular remodeling led to chronic heart failure. How to compensate the myocardium loss is a big obstacle that should be strode over by cardiologists. Over the past years, a variety of cell types, including fetus or adult cardiomyocytes, skeletal muscle satellite cells and embryonic stem cells, have been proposed as the candidates for cardiac celluar transplantation to augment heart function. But these cell types exist some problems such as ethics, immuno- suppression and donor source limitation. Bone mesenchymal stem cells constitute a separate group of stem cells other than hematopoietic stem cells in bone marrow. It were reported that under controlled conditions, MSCs have been reproducibly guided to differentiate into multiple mesenchymal lineages. But these reports have some diversity in the MSCs biological characteristics as morphology or surface markers. The factors or molecules involved in the differentiation program are unclear yet. More over, doubts are still shed on the transdifferentiation ability of MSCs.Data derived from animal experimental study and clinical obsrevation have demonstrated the feasibility of MSCs transplantation therapy for myocardium injury. After injection into the damaged region, MSCs incorporated and intergrated into native myocardial fibers and expressed cardiac specific markers and resulted in cardiac function improvement. However, some other research group reported that the graft cells do not expression cardiac markers unless MSCs treated by 5-azacytidine pre-transplantation. Therefore, more experiment evidence should be provided to confirm the hypothesis that MSCs could undergo milieu-dependent differentiation in the host heart tissue.The partial repair of the infracted heart implied that the transplanted cells responded to unknown molecular signals from the injured myocardium, such as inflammatory factors and/or cytokines, that promoted their survival, migration, proliferation and differentiation within the necrotic area of the ventricular wall. The studys on fetal development and embryonic stem cells (ESCs) differentiation demonstrated that stem cell factor (SCF) mediates the migration and/or differentiation of haematopoietic stem cells (HSCs) and other primitive cells to their target organs. But it is not clear whether adult heart cells generate SCF and act the similar roles on MSCs as that on ESCs.Recently, it was reported that stromal cell-derived factor-1 (SDF-1), a newly founded novel chemokine which belongs to the CXCR4 chemokine family, is crucial for bone marrow retention of HSCs and is involed in cardiogenesis, migration of primordial germ cells (PGCs), and recruitment of endothelial cell progenitor cells (EPCs) to sites of ischemic tissue. The relationship between SDF-1 and myocardium injury and the effect of SDF-1 on MSCs migration, retention and trans-differentiation is unknown either.It presumed that tissue environment dictated the fate changes of MSCs and MSCs trans-differentiated into the specified cells which surrounding them. There may give rise to another question whether MSCs undergo the same fate in co-culture system with cardiomyocytes in vitro as them in vivo or not. It is well-known that cardiomyocytes only counts one third of the whole cell population in heart, however, which type of these cells guide the reprogram of MSCs into cardiomyocytes?Based on its plasticity and abundance in bone marrow, MSCs may be a type of prospective engineering seed cells for tissue repair or cell and gene therapy for some gene deficiency diseases. The expression of the target exogenous gene and its effect on MSCs survival, proliferation and differentiation need urgently further study.Methods 1. Using the characteristics of anchorage-depend...
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