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轴突-施万细胞相互作用调节施万细胞中c-jun的表达。

Axon-Schwann cell interactions regulate the expression of c-jun in Schwann cells.

作者信息

Shy M E, Shi Y, Wrabetz L, Kamholz J, Scherer S S

机构信息

Department of Neurology, Wayne State University, Detroit, Michigan, USA.

出版信息

J Neurosci Res. 1996 Mar 1;43(5):511-25. doi: 10.1002/(SICI)1097-4547(19960301)43:5<511::AID-JNR1>3.0.CO;2-L.

Abstract

The transcription factor c-jun is selectively expressed by non-myelinating Schwann cells in normal peripheral nerve, and be "denervated," previously myelinatng Schwann cells, after axotomy. When axons regenerate into the distal nerve-stump, the expression of c-jun declines as Schwann cells remyelinate axons. Treating cultured Schwann cells with forskolin, a drug that mimics many of the effects of axon-Schwann cell interactions, decreases the expression of myelin-specific genes. Overexpressing c-jun in cultured Schwann cells, however, does not decrease the expression of a myelin basic protein promoter-reporter construct, indicating that c-jun expression may not directly regulate myelin-specific gene expression. These data suggest that c-jun is invloved in regulating the phenotype of non-myelinating and denervated Schwann cells.

摘要

转录因子c-jun在正常外周神经的非髓鞘形成施万细胞中选择性表达,并且在轴突切断后,由先前形成髓鞘的施万细胞“去神经支配”。当轴突再生进入远端神经残端时,随着施万细胞重新髓鞘化轴突,c-jun的表达下降。用福斯可林处理培养的施万细胞,福斯可林是一种模拟轴突与施万细胞相互作用的许多效应的药物,可降低髓鞘特异性基因的表达。然而,在培养的施万细胞中过表达c-jun并不会降低髓鞘碱性蛋白启动子-报告基因构建体的表达,这表明c-jun的表达可能不会直接调节髓鞘特异性基因的表达。这些数据表明c-jun参与调节非髓鞘形成和去神经支配的施万细胞的表型。

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