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脑周细胞在亨廷顿病中早期被激活。

Brain pericyte activation occurs early in Huntington's disease.

机构信息

Translational Neurology group, Department of Clinical Science, Wallenberg Neuroscience Center, Wallenberg Centre for Molecular Medicine at Lund University, Lund University, 22184 Lund, Sweden.

Neural Plasticity and Repair Unit, Department of Experimental Medical Science, Wallenberg Neuroscience Center, Lund University, 22184 Lund, Sweden.

出版信息

Exp Neurol. 2018 Jul;305:139-150. doi: 10.1016/j.expneurol.2018.03.015. Epub 2018 Apr 7.

Abstract

Microvascular changes have recently been described for several neurodegenerative disorders, including Huntington's disease (HD). HD is characterized by a progressive neuronal cell loss due to a mutation in the Huntingtin gene. However, the temporal and spatial microvascular alterations in HD remain unclear. Also, knowledge on the implication of pericytes in HD pathology is still sparse and existing findings are contradictory. Here we examine alterations in brain pericytes in the R6/2 mouse model of HD and in human post mortem HD brain sections. To specifically track activated pericytes, we crossbred R6/2 mice with transgenic mice expressing the Green fluorescent protein gene under the Regulator of G-protein signaling 5 (Rgs5) promoter. We demonstrate an increase in activated pericytes in the R6/2 brain and in post mortem HD brain tissue. Importantly, pericyte changes are already detected before striatal neuronal cell loss, weight loss or behavioural deficits occur in R6/2 mice. This is associated with vascular alterations, whereby striatal changes precede cortical changes. Our findings suggest that pericyte activation may be one of the initial steps contributing to the observed vascular modifications in HD. Thus, pericytes may constitute an important target to address early microvascular changes contributing to disease progression in HD.

摘要

微血管变化最近已被描述为几种神经退行性疾病,包括亨廷顿病(HD)。HD 的特征是由于亨廷顿基因的突变导致神经元进行性丧失。然而,HD 中的时空微血管改变仍不清楚。此外,关于周细胞在 HD 病理学中的作用的知识仍然很少,现有的发现存在矛盾。在这里,我们研究了 R6/2 小鼠 HD 模型和人类死后 HD 脑切片中脑周细胞的改变。为了专门追踪激活的周细胞,我们将 R6/2 小鼠与在 Rgs5 启动子下表达绿色荧光蛋白基因的转基因小鼠杂交。我们证明 R6/2 大脑和死后 HD 脑组织中激活的周细胞增加。重要的是,在 R6/2 小鼠出现纹状体神经元细胞丢失、体重减轻或行为缺陷之前,就已经检测到周细胞的变化。这与血管改变有关,纹状体的变化先于皮质的变化。我们的研究结果表明,周细胞激活可能是导致 HD 中观察到的血管改变的初始步骤之一。因此,周细胞可能是治疗 HD 中导致疾病进展的早期微血管变化的重要靶点。

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