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MicroRNA-9 induces defective trafficking of Nav1.1 and Nav1.2 by targeting Navβ2 protein coding region in rat with chronic brain hypoperfusion

机译:MicroRNA-9通过靶向慢性脑低灌注大鼠的Navβ2蛋白编码区诱导Nav1.1和Nav1.2的缺陷运输

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摘要

BackgroundPrevious studies have demonstrated that the trafficking defects of Nav1.1/Nav1.2 are involved in the dementia pathophysiology. However, the detailed mechanisms are not fully understood. Moreover, whether the impaired miRNAs regulation linked to dementia is a key player in sodium channel trafficking disturbance remains unclear. The cognitive impairment induced by chronic cerebral ischemia through chronic brain hypoperfusion (CBH) is likely reason to precede dementia. Therefore, our goal in the present study was to examine the role of microRNA-9 (miR-9) in regulating Nav1.1/Nav1.2 trafficking under CBH generated by bilateral common carotid artery occlusion (2VO).
机译:背景先前的研究表明Nav1.1 / Nav1.2的运输缺陷与痴呆的病理生理学有关。但是,详细的机制尚未完全理解。此外,与痴呆症相关的miRNAs调节受损是否是钠通道运输障碍的关键因素尚不清楚。由慢性脑低灌注(CBH)引起的慢性脑缺血引起的认知障碍可能是痴呆之前的原因。因此,我们在本研究中的目标是研究microRNA-9(miR-9)在调节由双侧颈总动脉闭塞(2VO)产生的CBH下Nav1.1 / Nav1.2转运中的作用。

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