Since B10 cells express c-kit, the receptor for SCF, CXCR4, the receptor for SDF-1, and VEGFR1, receptor for VEGF, pathways involving SCF/c-kit, SDF-1/ CXCR4 and VEGF/VEGFR are involved in the migration of MSCs to the sites of ICH brain damage and also to corpus callosum and hippocampus. Migration of MSCs toward sites of brain injury may represent an adaptive response of MSCs for the purpose of limiting tissue injury or repair the tissue damage. The mechanism by which the B10 MSCs undergo selective and long distance migration to non-injured sites of corpus callosum and hippocampus might differ from that for the ICH injury and further studies are required to identify the signal for the MSC migration to apparently normal brain region. Brain microenvironment is important in determining survival, migration and differentiation of exogenously transplanted progenitor cells and stem cells. Following the collagenase injection into the striatum, a profuse hemorrhage in the area caused by blood vessels damaged by the proteinase enzyme ensues and the hemorrhage core routinely is absorbed within a week or two, but immune cells released from the vessels remain in the hemorrhage core area. Transplantation of B10 human MSCs is conducted one week after the hemorrhage lesion, thus host immune cells might 4-(Benzyloxy)phenol attack the newly implanted human MSCs in the area. On the other hand, it is known that damaged brain cells and tissues of the host are also capable of releasing molecules that stimulate Amikacin hydrate production of neurotrophic factors in transplanted MSCs. In the present study, no immunosuppressant such as cyclosporine A was utilized to inhibit immune reaction and promote the long-term survival of implanted MSCs in the ICH animals. In earlier studies we have intravenously transplanted immortalized stable human neural stem cells in ICH and focal ischemia model rats without administering immunosuppressant, and found a good survival of grafted NSCs in the brain and a good functional recovery in these animals. However, low survival rate of grafted B10 cells in ICH mice as demonstrated in the present study is a grave concern. The survival rate of transplanted B10 cells at 2 weeks post-transplantation is 41% and that of 6 weeks is 20%. Obvious cause for such poor survival rate of human MSCs in experimental animals is immune-mediated mechanisms by which grafted cells were attacked and destroyed. For that reason, we have to employ immunosuppressants in our future studies to protect grafted human MSCs from cell death in experimental animals. It should be noted that the immunosuppressant cyclosporine has recently been demonstrated to exert neuroprotection in experimental stroke among other disease models. The importance of immunosuppresion in the event of clinical trials using human MSCs in patients suffering from stroke or other neurological diseases is well recognized. Immunological rejection of neural transplants poses a significant problem to be overcome in order to conduct successfully stem cell-based cell therapy in human patients. A previous study has suggested that the use of progenitors and stem cells for neural grafting is more promising, as these could be maintained in vitro until use, and evoke less immunogenic responses when compared to primary grafts; implantation of immortalized mouse neural stem cells in rat ischemia model has resulted in a good survival at 2 weeks posttransplantation in the absence of immune reaction caused by grafted cells. Further investigations into the specific mechanisms underlying drug actions of immunosuppressants in experimental stroke will certainly improve the therapeutic potential of these drugs for stem cell-based cell therapy.