Why do Schwann cells survive in the absence of axons?

被引:44
作者
Jessen, KR [1 ]
Mirsky, R [1 ]
机构
[1] UCL, Dept Anat & Dev Biol, London WC1E 6BT, England
来源
CHARCOT-MARIE-TOOTH DISORDERS | 1999年 / 883卷
基金
英国惠康基金;
关键词
D O I
10.1111/j.1749-6632.1999.tb08573.x
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Schwann cell precursors in embryonic nerves rely for survival on signals from the axons they associate with. A major component of this signal is beta neuregulin. While it can be argued that such paracrine axonal regulation makes biological sense in embryonic nerves, such an arrangement would be problematic postnatally, since nerve damage would then lead to Schwann cell death with adverse consequences for regeneration; in fact, transection of older nerves is not accompanied by a detectable increase in Schwann cell death. Our evidence indicates that this is, at least in part, due to the ability of Schwann cells to support their own survival by autocrine circuits. These circuits are not present in Schwann cell precursors. me have identified insulin like growth factor, neurotrophin-3 and platelet-derived growth factor BB as components of the autocrine Schwann cell survival signal.
引用
收藏
页码:109 / 115
页数:7
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