Chemokine CXCL12 in neurodegenerative diseases: an SOS signal for stem cell-based repair

被引:82
作者
Li, Meizhang [1 ,2 ]
Hale, James S. [1 ]
Rich, Jeremy N. [2 ,3 ]
Ransohoff, Richard M. [4 ]
Lathia, Justin D. [1 ,2 ,3 ]
机构
[1] Cleveland Clin, Lerner Res Inst, Dept Cell Biol, Cleveland, OH 44106 USA
[2] Cleveland Clin, Lerner Res Inst, Dept Stem Cell Biol & Regenerat Med, Cleveland, OH 44106 USA
[3] Case Western Reserve Univ, Case Comprehens Canc Ctr, Cleveland, OH 44106 USA
[4] Cleveland Clin, Lerner Res Inst, Dept Neurosci, Cleveland, OH 44106 USA
基金
美国国家卫生研究院;
关键词
CXCL12; CXCR4; neurodegeneration; stem cells; tissue repair; NEURAL PROGENITOR CELLS; PRIMITIVE HEMATOPOIETIC-CELLS; POSTNATAL DENTATE GYRUS; BONE-MARROW; SUBVENTRICULAR ZONE; VASCULAR NICHE; RECEPTOR CXCR4; FACTOR-I; MULTIPLE-SCLEROSIS; ALZHEIMERS-DISEASE;
D O I
10.1016/j.tins.2012.06.003
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The dynamic relation between stem cells and their niche governs self-renewal and progenitor cell deployment. The chemokine CXCL12 (C-X-C motif ligand 12) and its signaling receptor CXCR4 (C-X-C motif receptor 4) represent an important pathway that regulates homing and maintenance of stem cells in neural niches. Neural stem cells (NSCs) reside in specific niches where communication with blood vessels is regulated by CXCL12. In neurodegenerative diseases and brain tumors, reactive vasculature forms in response to diseased tissues to create new niches that secrete CXCL12, enhancing the recruitment of neural progenitor cells (NPCs) to lesion sites via long-range migration. These observations suggest that the CXCL12 CXCR4 axis maintains NSCs and serves as an emergent salvage signal for initiating endogenous stem cell-based tissue repair.
引用
收藏
页码:619 / 628
页数:10
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