Axonal signals regulate expression of glia maturation factor-beta in Schwann cells: an immunohistochemical study of injured sciatic nerves and cultured Schwann cells
Axonal signals regulate expression of glia maturation factor-beta in Schwann cells: an immunohistochemical study of injured sciatic nerves and cultured Schwann cells
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DOI：
10.1523/jneurosci.09-10-03690.1989
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发表时间：
1989-10
期刊：
影响因子：
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通讯作者：
E. Bosch;W. Zhong;R. Lim
中科院分区：
文献类型：
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作者：
E. Bosch;W. Zhong;R. Lim
胶质成熟因子-β（GMF-β）是从牛脑中纯化并测序的17 kDa蛋白质。使用针对GMF-β的单克隆抗体G2-09，我们先前证明了成星形细胞、许旺细胞及其培养的肿瘤中的内源性GMF-β。在本研究中，我们已经使用间接免疫荧光显微镜与G2-09检查坐骨神经的横断，挤压和再生对施旺细胞中GMF-β原位表达的影响，并在体外研究施旺细胞中GMF-β诱导的时间过程。为了比较，用针对神经生长因子（NGF）受体的单克隆抗体进行了平行研究。我们发现：（1）在完整的坐骨神经中，GMF-β和NGF受体均未检测到;（2）切断神经远段的所有雪旺细胞早在切断后3天就表达GMF-β，并持续长达3周;（3）轴突再生抑制雪旺细胞表达GMF-β，（4）来源于大鼠坐骨神经和成人腓肠神经的分离的施万细胞在培养物中在初始滞后期后产生细胞内GMF-β，（5）在切断的神经和培养的神经中，雪旺细胞NGF受体的诱导与GMF-β的诱导在时间上一致。这些结果表明，与NGF受体的情况一样，施旺细胞中GMF-β的表达是由正常轴突-施旺细胞接触的丧失诱导的。我们认为，神经损伤后雪旺细胞中GMF-β和NGF受体的诱导在轴突再生中起作用。
Glia maturation factor-beta (GMF-beta) is a 17 kDa protein purified and sequenced from bovine brains. Using the monoclonal antibody G2–09 directed against GMF-beta, we previously demonstrated endogenous GMF- beta in astroblasts, Schwann cells, and their tumors in culture. In the present study, we have used indirect immunofluorescence microscopy with G2–09 to examine the effects of transection, crush, and regeneration of sciatic nerve on the expression of GMF-beta in Schwann cells in situ and to study the time course of GMF-beta induction in Schwann cells in vitro. For comparison, a parallel study was carried out with monoclonal antibodies directed against nerve growth factor (NGF) receptor. We found that (1) neither GMF-beta nor NGF receptor was detectable in intact sciatic nerves, (2) all Schwann cells of the distal segment of the transected nerve expressed GMF-beta as early as 3 d after axotomy that persisted up to 3 weeks, (3) axonal regeneration repressed the Schwann cell expression of GMF-beta, (4) isolated Schwann cells derived from rat sciatic and adult human sural nerves developed intracellular GMF-beta in culture following an initial lag period, and (5) the induction of Schwann cell NGF receptor coincided temporally with that of GMF-beta in the transected nerve and in culture. These results show that the expression of GMF-beta in Schwann cells, as is the case with the NGF receptor, is induced by the loss of the normal axon-Schwann cell contact. We propose that the induction of GMF-beta, as well as NGF receptor, in Schwann cells after nerve injury plays a role in axonal regeneration.