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人脑胶质母细胞瘤中紊乱的血脑屏障。

The disturbed blood-brain barrier in human glioblastoma.

机构信息

Department of General Pathology and Pathological Anatomy, Institute of Pathology and Neuropathology, University of Tübingen, Tübingen, Germany.

出版信息

Mol Aspects Med. 2012 Oct-Dec;33(5-6):579-89. doi: 10.1016/j.mam.2012.02.003. Epub 2012 Feb 23.

Abstract

The aim of this article is to describe alterations of the blood-brain barrier (BBB) in gliomas. The main clinical problem of human gliomas is the edematous swelling and the dramatic increase of intracerebral pressure, also compromising healthy areas of the brain. According to our concept, one of the main reasons on the cellular level for these clinical problems is the loss or reduction of astroglial polarity. Astroglial polarity means the specific accumulation of potassium and water channels in the superficial and perivascular astroglial endfeet membranes. The most important water channel in the CNS is the astroglial water channel protein aquaporin-4 (AQP4) which is arranged in a morphologically spectacular way, the so-called orthogonal arrays of particles (OAPs) to be observed in freeze-fracture replicas. In brain tumors, but also under conditions of trauma or inflammation, these OAPs are redistributed to membrane domains apart from endfeet areas. Probably, this dislocation might be due to the degradation of the proteoglycan agrin by the matrix metalloproteinase 3 (MMP3). Agrin binds to the dystrophin-dystroglycan-complex (DDC), which in turn is connected to AQP4. As a consequence, agrin loss may lead to a redistribution of AQP4 and a compromised directionality of water transport out of the cell, finally to cytotoxic edema. This in turn is hypothesized to lead to a breakdown of the BBB characterized by disturbed tight junctions, and thus to the development of vasogenic edema. However, the mechanism how the loss of polarity is related to the disturbance of microvascular tight junctions is completely unknown so far.

摘要

本文旨在描述血脑屏障 (BBB) 在神经胶质瘤中的改变。人类神经胶质瘤的主要临床问题是水肿和颅内压的急剧升高,这也会影响大脑的健康区域。根据我们的概念,这些临床问题在细胞水平上的主要原因之一是星形胶质细胞极性的丧失或减少。星形胶质细胞极性是指钾离子和水通道在浅层和血管周围星形胶质细胞足突膜中的特异性积累。CNS 中最重要的水通道是星形胶质细胞水通道蛋白 aquaporin-4 (AQP4),它以一种形态学上引人注目的方式排列,即所谓的冷冻断裂复制品中观察到的正交颗粒排列 (OAPs)。在脑肿瘤中,但在创伤或炎症条件下,这些 OAPs 会重新分布到远离足突区域的膜域。可能,这种重定位是由于基质金属蛋白酶 3 (MMP3) 降解了糖胺聚糖核心蛋白聚糖 agrin。Agrin 与 dystrophin-dystroglycan-complex (DDC) 结合,而 DDC 又与 AQP4 相连。因此,agrin 的丢失可能导致 AQP4 的重新分布和细胞内水运输方向的受损,最终导致细胞毒性水肿。反过来,这被假设为 BBB 的破坏导致,其特征是紧密连接紊乱,从而导致血管源性水肿的发展。然而,极性丧失与微血管紧密连接紊乱之间的关系的机制目前尚完全不清楚。

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