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Open Access Highly Accessed Research article

Transplanted bone marrow stem cells relocate to infarct penumbra and co-express endogenous proliferative and immature neuronal markers in a mouse model of ischemic cerebral stroke

Xue-mei Zhang1, Fang Du1, Dan Yang1, Chun-jiang Yu1, Xiang-nan Huang1, Wei Liu2 and Jin Fu1*

Author affiliations

1 Department of Neurology, The Second Affiliated Hospital, Harbin Medical University, Harbin, 150086, China

2 Center of Research and Experiment, The Second Affiliated Hospital, Harbin Medical University, Harbin, 150086, China

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Citation and License

BMC Neuroscience 2010, 11:138  doi:10.1186/1471-2202-11-138

Published: 25 October 2010

Abstract

Background

Several studies demonstrate that neurogenesis may be induced or activated following vascular insults, which may be important for neuronal regeneration and functional recovery. Understanding the cellular mechanism underlying stroke-associated neurogenesis is of neurobiological as well as neurological/clinical relevance. The present study attempted to explore potential homing and early development of transplanted bone marrow stem cells in mouse forebrain after focal occlusion of the middle cerebral artery, an experimental model of ischemic stroke.

Results

Bone marrow stem cells isolated from donor mice were confirmed by analysis of surface antigen profile, and were pre-labeled with a lipophilic fluorescent dye PKH26, and subsequently transfused into recipient mice with middle cerebral artery coagulation. A large number of PKH26-labeled cells were detected surrounding the infarct site, most of which colocalized with immunolabelings for the proliferating cell nuclear antigen (PCNA) and some also colocalized with the immature neuronal marker doublecortin (DCX) during 1-2 weeks after the bone marrow cells transfusion.

Conclusions

The present study shows that transplanted bone morrow cells largely relocate to the infarct penumbra in ischemic mouse cerebrum. These transplanted bone marrow cells appear to undergo a process of in situ proliferation and develop into putative cortical interneurons during the early phase of experimental vascular injury.