BACKGROUND Accumulating evidence has documented that microRNA-7 (miR-7) plays an important role in the pathology of various diseases. However, the potential role of miR-7 in brain tissue inflammation (BTI) remains unclear. METHODS We detected the expression of miR-7 in LPS-induced murine BTI model and observed the possible effects of miR-7 deficiency on the pathology of BTI. To elucidate the mechanism, the target gene of miR-7 was screened out by Gene chip assay and its potential roles in BTI were evaluated by Western blot, immunofluorescence, and RNAi assay, respectively. RESULTS MiR-7 was upregulated in brain tissue in BTI mice and its deficiency could significantly aggravate the pathology of brain tissue. Moreover, RORα, a new target molecule of miR-7, was upregulated in brain tissue from miR-7 deficiency BTI mice. Of note, downregulation of RORα could remarkably exacerbate the pathology of brain tissue and elevate the transduction of NF-κB and ERK1/2 signaling pathways in brain tissue from miR-7 deficiency BTI mice. Furthermore, RORα and miR-7 were dominantly co-expressed in neurons of BTI mice. Finally, RORα synergized with miR-7 to control the inflammatory reaction of neuronal cells in response to LPS stimulation. CONCLUSIONS MiR-7 expression is upregulated in BTI model. Moreover, miR-7 synergizes with its target gene RORα to control the inflammation reaction of neurons, thereby orchestrating the pathology of BTI.

中文翻译：

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MicroRNA-7与RORα协同作用，负面控制脑组织炎症的病理。

背景技术越来越多的证据表明，microRNA-7（miR-7）在各种疾病的病理学中起着重要作用。但是，尚不清楚miR-7在脑组织炎症（BTI）中的潜在作用。方法我们检测了LPS诱导的鼠BTI模型中miR-7的表达，并观察了miR-7缺乏对BTI病理的影响。为了阐明机理，通过基因芯片分析筛选出miR-7的靶基因，并分别通过蛋白质印迹，免疫荧光和RNAi分析评估其在BTI中的潜在作用。结果BTI小鼠脑组织中的MiR-7上调，其缺乏可能显着加重脑组织的病理。此外，miR-7缺陷BTI小鼠的脑组织中的miR-7的新靶分子RORα被上调。值得注意的是 RORα的下调可显着加重miR-7缺陷BTI小鼠脑组织的病理，并提高NF-κB和ERK1 / 2信号通路在脑组织中的转导。此外，RORα和miR-7在BTI小鼠的神经元中显着共表达。最后，RORα与miR-7协同控制神经细胞对LPS刺激的炎症反应。结论在BTI模型中MiR-7表达被上调。而且，miR-7与它的靶基因RORα协同控制神经元的炎症反应，从而协调BTI的病理。RORα和miR-7在BTI小鼠的神经元中显着共表达。最后，RORα与miR-7协同控制神经元细胞对LPS刺激的炎症反应。结论在BTI模型中MiR-7表达被上调。而且，miR-7与它的靶基因RORα协同控制神经元的炎症反应，从而协调BTI的病理。RORα和miR-7在BTI小鼠的神经元中显着共表达。最后，RORα与miR-7协同控制神经元细胞对LPS刺激的炎症反应。结论在BTI模型中MiR-7表达被上调。而且，miR-7与它的靶基因RORα协同控制神经元的炎症反应，从而协调BTI的病理。