TY - JOUR
T1 - Mechanisms underlying intravenous transplantation of human amniotic mesenchymal stem cells for Alzheimer's disease in transgenic APP+ mice
AU - Wang, Cheng Chun
AU - Bo, Yang
AU - Guan, Fang Xia
AU - Li, Guo Dong
AU - Zhou, Chang Hui
AU - Zhou, Yun Fan
AU - Xiang, Hu
AU - Gu, Chen Xi
AU - Lei, Ning Jing
PY - 2010/5/7
Y1 - 2010/5/7
N2 - BACKGROUND: APP gene is closely associated with the onset of Alzheimer' disease. Intravenous transplantation of human amniotic mesenchymal stem cell (AMSCs) can promote the learning and memory improvement in transgenic APP+ mice with Alzheimer' disease. OBJECTIVE: To study whether the AMSCs can transfer into the brain tissue of Alzheimer's disease mice, and differentiate into the neural cell, then cure the disease after the human AMSC transplantation via tail venous injection. METHODS: Human AMSCs were isolated in vitro sterilely. At the third passage, 0.5 mL single cell suspension at 1 × 109/L was obtained and transplanted by tail venous pathway in transplantation group mice, Mice in the control group were injected with an equal volume of saline. APP-gene mice in the normal group were left intact. 5′-bromo-2-deoxyuridine (BrdU) labeled third-generation AMSCs expression was detected in mice brain tissue by immunohistochemical method. Glial fibrillary acidic protein (GFAP), Nestin and neuron specific enolase (NSE) expression was measured in the brain tissue of mice from each group. RESULTS AND CONCLUSION: Under an optical microscope, a majority of nuclei in the brain tissue of mice from transplantation group were stained blue, but some nuclei were stained brown, positive for BrdU. Compared with control group, the expression of GFAP in the brain tissue of transplanted mice was increased about 4 times, even more than in the normal group (P < 0.05). The expression of Nestin in the brain tissue of transplanted mice was increased about 10%, but still lower than the normal group nearly 20% (P < 0.05). NSE expression was decreased by 1/3, but still higher compared with the normal group (P < 0.05). Above-mentioned results have shown that human AMSC transplantation for treating Alzheimer's disease takes place by AMSCs homing to APP+ mouse brain tissue and differentiating into neural cells.
AB - BACKGROUND: APP gene is closely associated with the onset of Alzheimer' disease. Intravenous transplantation of human amniotic mesenchymal stem cell (AMSCs) can promote the learning and memory improvement in transgenic APP+ mice with Alzheimer' disease. OBJECTIVE: To study whether the AMSCs can transfer into the brain tissue of Alzheimer's disease mice, and differentiate into the neural cell, then cure the disease after the human AMSC transplantation via tail venous injection. METHODS: Human AMSCs were isolated in vitro sterilely. At the third passage, 0.5 mL single cell suspension at 1 × 109/L was obtained and transplanted by tail venous pathway in transplantation group mice, Mice in the control group were injected with an equal volume of saline. APP-gene mice in the normal group were left intact. 5′-bromo-2-deoxyuridine (BrdU) labeled third-generation AMSCs expression was detected in mice brain tissue by immunohistochemical method. Glial fibrillary acidic protein (GFAP), Nestin and neuron specific enolase (NSE) expression was measured in the brain tissue of mice from each group. RESULTS AND CONCLUSION: Under an optical microscope, a majority of nuclei in the brain tissue of mice from transplantation group were stained blue, but some nuclei were stained brown, positive for BrdU. Compared with control group, the expression of GFAP in the brain tissue of transplanted mice was increased about 4 times, even more than in the normal group (P < 0.05). The expression of Nestin in the brain tissue of transplanted mice was increased about 10%, but still lower than the normal group nearly 20% (P < 0.05). NSE expression was decreased by 1/3, but still higher compared with the normal group (P < 0.05). Above-mentioned results have shown that human AMSC transplantation for treating Alzheimer's disease takes place by AMSCs homing to APP+ mouse brain tissue and differentiating into neural cells.
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U2 - 10.3969/j.issn.1673-8225.2010.19.011
DO - 10.3969/j.issn.1673-8225.2010.19.011
M3 - Article
AN - SCOPUS:77955046340
SN - 1673-8225
VL - 14
SP - 3471
EP - 3476
JO - Journal of Clinical Rehabilitative Tissue Engineering Research
JF - Journal of Clinical Rehabilitative Tissue Engineering Research
IS - 19
ER -
