期刊
CELLULAR AND MOLECULAR NEUROBIOLOGY
卷 35, 期 7, 页码 913-920出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10571-015-0186-6
关键词
Basic fibroblast growth factor; Pre-oligodendrocyte; Oxygen/glucose deprivation; Hypoxia-ischemia; Demyelination; Fibroblast growth factor receptor 3
资金
- National Natural Science Foundation of China [81271345, 81302519]
- Natural Science Foundation of Jiangsu Province [BK20131132, BK20130221]
- Qing Lan Project of Jiangsu Province
- Xuzhou Project of Science and Technology for Social Development [XZZD1324]
- College Graduate Research and Innovation Project of Jiangsu Province [CXZZ13_0983]
One of the pathological hallmarks of periventricular white matter injury is the vulnerability of pre-oligodendrocytes (preOLs) to hypoxia-ischemia (HI). There is increasing evidence that basic fibroblast growth factor (bFGF) is an important signaling molecule for neurogenesis and neuroprotection in the central nervous system. However, it is unknown whether bFGF protects preOLs from oxygen/glucose deprivation (OGD) damage in vitro and promotes remyelination in HI-induced rats. In this present study, bFGF exerted a protective effect on myelin by increasing the myelin thickness, the number of myelinated axons, and myelin basic protein expression in the HI-induced demyelinated neonatal rat corpus callosum. In vitro, bFGF ameliorated the impaired mitochondria and cell processes induced by OGD to promote the survival of isolated O4-positive preOLs. Additionally, the expression of fibroblast growth factor receptor 3 (FGFR3) was dramatically up-regulated in the preOLs after bFGF administration in vivo and in vitro. Thus, bFGF-stimulated remyelination in HI-induced rats by protecting the preOLs from hypoxic injury, and the mechanism involved may be mediated by FGFR3.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据