Fas engagement induces neurite growth through ERK activation and p35 upregulation

被引:252
作者
Desbarats, J
Birge, RB
Mimouni-Rongy, M
Weinstein, DE
Palerme, JS
Newell, MK
机构
[1] McGill Univ, Dept Physiol, Montreal, PQ H3G 1Y6, Canada
[2] Rockefeller Univ, Oncol Mol Lab, New York, NY 10021 USA
[3] Univ Colorado, Dept Biol, Colorado Springs, CO 80918 USA
[4] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Biochem & Mol Biol, Newark, NJ 07103 USA
[5] Yeshiva Univ Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA
[6] Yeshiva Univ Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10461 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1038/ncb916
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Fas (also known as CD95), a member of the tumour-necrosis receptor factor family of 'death receptors', can induce apoptosis or, conversely, can deliver growth stimulatory signals. Here we report that crosslinking Fas on primary sensory neurons induces neurite growth through sustained activation of the extracellular-signal regulated kinase (ERK) pathway and the consequent upregulation of p35, a mediator of neurite outgrowth. In addition, functional recovery after sciatic nerve injury is delayed in Fas-deficient lpr mice and accelerated by local administration of antibodies against Fas, which indicates that Fas engagement may contribute to nerve regeneration in vivo. Our findings define a role for Fas as an inducer of both neurite growth in vitro and accelerated recovery after nerve injury in vivo.
引用
收藏
页码:118 / 125
页数:8
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