Mechanisms underlying intravenous transplantation of human amniotic mesenchymal stem cells for Alzheimer's disease in transgenic APP+ mice

Cheng Chun Wang, Yang Bo, Fangxia Guan, Guo Dong Li, Chang Hui Zhou, Yun Fan Zhou, Hu Xiang, Chen Xi Gu, Ning Jing Lei

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)3471-3476
Number of pages6
JournalJournal of Clinical Rehabilitative Tissue Engineering Research
Volume14
Issue number19
DOIs
StatePublished - May 7 2010
Externally publishedYes

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Stem cells
Mesenchymal Stromal Cells
Transgenic Mice
Brain
Alzheimer Disease
Transplantation
Tissue
Nestin
Phosphopyruvate Hydratase
Glial Fibrillary Acidic Protein
Bromodeoxyuridine
Mesenchymal Stem Cell Transplantation
Neurons
Genes
Proteins
Brain Tissue Transplantation
Tail
Control Groups
Suspensions
Microscopes

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Biomedical Engineering
  • Transplantation

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Mechanisms underlying intravenous transplantation of human amniotic mesenchymal stem cells for Alzheimer's disease in transgenic APP+ mice. / Wang, Cheng Chun; Bo, Yang; Guan, Fangxia; Li, Guo Dong; Zhou, Chang Hui; Zhou, Yun Fan; Xiang, Hu; Gu, Chen Xi; Lei, Ning Jing.

In: Journal of Clinical Rehabilitative Tissue Engineering Research, Vol. 14, No. 19, 07.05.2010, p. 3471-3476.

Research output: Contribution to journalArticle

Wang, Cheng Chun ; Bo, Yang ; Guan, Fangxia ; Li, Guo Dong ; Zhou, Chang Hui ; Zhou, Yun Fan ; Xiang, Hu ; Gu, Chen Xi ; Lei, Ning Jing. / Mechanisms underlying intravenous transplantation of human amniotic mesenchymal stem cells for Alzheimer's disease in transgenic APP+ mice. In: Journal of Clinical Rehabilitative Tissue Engineering Research. 2010 ; Vol. 14, No. 19. pp. 3471-3476.
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abstract = "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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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, Fangxia

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

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