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Human Gene Therapy
Neurodegeneration Augments the Ability of Bone Marrow-Derived Mesenchymal Stem Cells to Fuse with Purkinje Neurons in Niemann–Pick Type C Mice

To cite this article:
Jae-Sung Bae, Shigeki Furuya, Yoko Shinoda, Shogo Endo, Edward H. Schuchman, Yoshio Hirabayashi, Hee Kyung Jin. Human Gene Therapy. August 2005, 16(8): 1006-1011. doi:10.1089/hum.2005.16.1006.

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Jae-Sung Bae
College of Veterinary Medicine, Kyungpook National University, Daegu 702-701, South Korea.
Shigeki Furuya
Neuronal Circuit Mechanisms Research Group, RIKEN Brain Science Institute, Saitama 351-0198, Japan.
Yoko Shinoda
Neuronal Circuit Mechanisms Research Group, RIKEN Brain Science Institute, Saitama 351-0198, Japan.
Shogo Endo
Laboratory for Learning and Memory, RIKEN Brain Science Institute, Saitama 351-0198, Japan.
Edward H. Schuchman
Department of Human Genetics and Carl C. Icahn Institute for Gene Therapy and Molecular Medicine, Mount Sinai School of Medicine, New York, NY 10029.
Yoshio Hirabayashi
Neuronal Circuit Mechanisms Research Group, RIKEN Brain Science Institute, Saitama 351-0198, Japan.
Dr. Hee Kyung Jin
College of Veterinary Medicine, Kyungpook National University, Daegu 702-701, South Korea.
Pain and Neural Injury Research Center, MRC, Kyungpook National University, Daegu 702-701, South Korea.

After transplantation, adult bone marrow-derived mesenchymal stem cells (BM-MSCs) may undergo transdifferentiation and/or cell fusion in response to new environments. However, the mechanism(s) that govern these cell fate switches remain unknown. Here we demonstrate that the pathology associated with murine Niemann– Pick disease type C (NP-C) cerebellum augments the ability of BM-MSCs to fuse with Purkinje neurons. The results suggest that the degenerative microenvironment of Purkinje neurons in the NP-C cerebellum modulates the cell fate switch of BM-MSCs via cell fusion.

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