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

机译:JunB是去极化大鼠脑神经元中MMP-9转录的阻遏物

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摘要

Matrix Metalloproteinase-9 (MMP-9) is an extracellularly operating enzyme involved in the synapticplasticity, hippocampal-dependent long term memory and neurodegeneration. Previous studies have shownits upregulation following seizure-evoking stimuli. Herein, we show that in the rat brain, MMP-9 mRNAexpression in response to pentylenetetrazole-evoked neuronal depolarization is transient. Furthermore, wedemonstrate 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 ratMMP-9 gene promoter in vivo. Surprisingly, manipulations with JunB expression levels in activated neuronsrevealed its moderate repressive action onto MMP-9 gene expression. Therefore, our study documents theactive repressive influence of AP-1 onto MMP-9 transcriptional regulation by the engagement of JunB.
机译:基质金属蛋白酶9(MMP-9)是一种细胞外操作酶,参与突触可塑性,海马依赖性长期记忆和神经退行性变。先前的研究表明其在诱发癫痫发作的刺激后上调。在这里,我们表明,在大鼠脑中,响应戊戊四唑引起的神经元去极化的MMP-9 mRNA表达是瞬时的。此外,我们证明,在大鼠海马中,神经元活化强烈诱导JunB表达,同时导致JunB / FosB复合体在体内在大鼠MMP-9基因启动子的-88 / -80 bp位点积累。出人意料的是,在激活的神经元中用JunB表达水平进行的操作揭示了其对MMP-9基因表达的中等抑制作用。因此,我们的研究记录了通过JunB的参与,AP-1对MMP-9转录调控的积极抑制作用。

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