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JunB是去极化大鼠脑神经元中基质金属蛋白酶-9转录的抑制因子。

JunB is a repressor of MMP-9 transcription in depolarized rat brain neurons.

作者信息

Rylski Marcin, Amborska Renata, Zybura Katarzyna, Michaluk Piotr, Bielinska Beata, Konopacki Filip A, Wilczynski Grzegorz M, Kaczmarek Leszek

机构信息

Department of Molecular and Cellular Neurobiology, Nencki Institute, Pasteura 3, 02-093 Warsaw, Poland.

出版信息

Mol Cell Neurosci. 2009 Jan;40(1):98-110. doi: 10.1016/j.mcn.2008.09.005. Epub 2008 Oct 11.

Abstract

Matrix Metalloproteinase-9 (MMP-9) is an extracellularly operating enzyme involved in the synaptic plasticity, hippocampal-dependent long term memory and neurodegeneration. Previous studies have shown its upregulation following seizure-evoking stimuli. Herein, we show that in the rat brain, MMP-9 mRNA expression in response to pentylenetetrazole-evoked neuronal depolarization is transient. Furthermore, we demonstrate that in the rat hippocampus neuronal activation strongly induces JunB expression, simultaneously leading to an accumulation of JunB/FosB complexes onto the -88/-80 bp site of the rat MMP-9 gene promoter in vivo. Surprisingly, manipulations with JunB expression levels in activated neurons revealed its moderate repressive action onto MMP-9 gene expression. Therefore, our study documents the active repressive influence of AP-1 onto MMP-9 transcriptional regulation by the engagement of JunB.

摘要

基质金属蛋白酶-9(MMP-9)是一种参与突触可塑性、海马依赖性长期记忆和神经退行性变的细胞外作用酶。先前的研究表明,在诱发癫痫的刺激后其表达上调。在此,我们表明,在大鼠脑中,对戊四氮诱发的神经元去极化反应时,MMP-9 mRNA表达是短暂的。此外,我们证明,在大鼠海马中,神经元激活强烈诱导JunB表达,同时导致JunB/FosB复合物在体内大鼠MMP-9基因启动子的-88/-80 bp位点上积累。令人惊讶的是,对激活神经元中JunB表达水平的操作揭示了其对MMP-9基因表达的适度抑制作用。因此,我们的研究记录了AP-1通过JunB的参与对MMP-9转录调控的积极抑制影响。

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