Schwannoma-derived growth factor promotes the neuronal differentiation and survival of PC12 cells.

Schwannoma-derived growth factor promotes the neuronal differentiation and survival of PC12 cells.
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DOI:
10.1083/jcb.116.3.777
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发表时间:
1992-02
影响因子:
7.8
通讯作者:
Schubert, D
Schubert, D
中科院分区:
生物学1区
文献类型:
--
作者:
Kimura, H;Schubert, D

文献摘要

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神经鞘瘤衍生生长因子(SDGF)最初是从神经鞘瘤细胞中分离出来的,作为神经胶质细胞和成纤维细胞的丝裂原。目前的数据表明,SDGF引起大鼠PC12细胞的形态和分子分化的方式类似于神经生长因子(NGF),但与之不同。它还能促进PC12在无血清条件下的存活。SDGF诱导的变化包括神经突的生长和GAP-43和转蛋白mrna的诱导,这些蛋白在轴突中高度表达。此外,SDGF和NGF都能诱导转录因子NGFI-A。SDGF反应的时间过程与NGF相似。地塞米松可抑制SDGF和NGF对Gap-43 mRNA的诱导,但对NGFI-A mRNA的合成无影响。这些观察结果表明,SDGF除了对胶质细胞和成纤维细胞具有促有丝分裂活性外,还对PC12细胞具有促进分化和存活的作用。
Schwannoma-derived growth factor (SDGF) was initially isolated from schwannoma cells as a mitogen for glial cells and fibroblasts. The present data show that SDGF causes the morphological and molecular differentiation of rat PC12 cells in a manner similar to, but distinguishable from nerve growth factor (NGF). It also promotes PC12 survival in serum-free conditions. SDGF induced changes include neurite outgrowth and the induction of the mRNAs for GAP-43 and transin, proteins which are highly expressed in axons. In addition, both SDGF and NGF induce the transcription factor, NGFI-A. The time course of the response to SDGF is similar to that for NGF. Gap-43 mRNA induction by both SDGF and NGF is inhibited by dexamethasone, but dexamethasone has no effect on NGFI-A mRNA synthesis. These observations show that SDGF has a differentiation and survival promoting effect on PC12 cells in addition to its mitogenic activity on glial cells and fibroblasts.