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神经退行性变增强了骨髓间充质干细胞与尼曼-匹克C型小鼠浦肯野神经元融合的能力。

Neurodegeneration augments the ability of bone marrow-derived mesenchymal stem cells to fuse with Purkinje neurons in Niemann-Pick type C mice.

作者信息

Bae Jae-Sung, Furuya Shigeki, Shinoda Yoko, Endo Shogo, Schuchman Edward H, Hirabayashi Yoshio, Jin Hee Kyung

机构信息

College of Veterinary Medicine, Kyungpook National University, Daegu, South Korea.

出版信息

Hum Gene Ther. 2005 Aug;16(8):1006-11. doi: 10.1089/hum.2005.16.1006.

Abstract

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.

摘要

移植后,成年骨髓来源的间充质干细胞(BM-MSCs)可能会响应新环境而发生转分化和/或细胞融合。然而,控制这些细胞命运转变的机制仍然未知。在这里,我们证明与小鼠C型尼曼-匹克病(NP-C)小脑相关的病理学增强了BM-MSCs与浦肯野神经元融合的能力。结果表明,NP-C小脑中浦肯野神经元的退行性微环境通过细胞融合调节BM-MSCs的细胞命运转变。

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