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海马硬化症中海马细胞外基质的重组。

Reorganization of the Brain Extracellular Matrix in Hippocampal Sclerosis.

机构信息

Department of Neurology, University Hospital Centre Zagreb, 10000 Zagreb, Croatia.

Department of Biology, School of Medicine, University of Zagreb, 10000 Zagreb, Croatia.

出版信息

Int J Mol Sci. 2022 Jul 25;23(15):8197. doi: 10.3390/ijms23158197.

DOI:10.3390/ijms23158197
PMID:35897768
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9332352/
Abstract

The extracellular matrix (ECM) is an important regulator of excitability and synaptic plasticity, especially in its highly condensed form, the perineuronal nets (PNN). In patients with drug-resistant mesial temporal lobe epilepsy (MTLE), hippocampal sclerosis type 1 (HS1) is the most common histopathological finding. This study aimed to evaluate the ECM profile of HS1 in surgically treated drug-resistant patients with MTLE in correlation to clinical findings. Hippocampal sections were immunohistochemically stained for aggrecan, neurocan, versican, chondroitin-sulfate (CS56), fibronectin, Wisteria floribunda agglutinin (WFA), a nuclear neuronal marker (NeuN), parvalbumin (PV), and glial-fibrillary-acidic-protein (GFAP). In HS1, besides the reduced number of neurons and astrogliosis, we found a significantly changed expression pattern of versican, neurocan, aggrecan, WFA-specific glycosylation, and a reduced number of PNNs. Patients with a lower number of epileptic episodes had a less intense diffuse WFA staining in (CA) fields. Our findings suggest that PNN reduction, changed ECM protein, and glycosylation expression pattern in HS1 might be involved in the pathogenesis and persistence of drug-resistant MTLE by contributing to the increase of CA pyramidal neurons' excitability. This research corroborates the validity of ECM molecules and their modulators as a potential target for the development of new therapeutic approaches to drug-resistant epilepsy.

摘要

细胞外基质 (ECM) 是兴奋性和突触可塑性的重要调节剂，尤其是在其高度浓缩的形式——神经周围网络 (PNN) 中。在耐药性颞叶内侧癫痫 (MTLE) 患者中，海马硬化 1 型 (HS1) 是最常见的组织病理学发现。本研究旨在评估 HS1 的 ECM 谱在与临床发现相关的耐药性 MTLE 手术治疗患者中的变化。对海马切片进行免疫组织化学染色，以检测聚集蛋白聚糖、神经蛋白聚糖、 versican、软骨素硫酸盐 (CS56)、纤连蛋白、Wisteria floribunda 凝集素 (WFA)、核神经元标志物 (NeuN)、parvalbumin (PV) 和胶质纤维酸性蛋白 (GFAP)。在 HS1 中，除了神经元数量减少和星形胶质细胞增生外，我们还发现 versican、神经蛋白聚糖、聚集蛋白聚糖、WFA 特异性糖基化的表达模式发生了显著变化，并且 PNN 的数量减少。癫痫发作次数较少的患者，在 CA 区域的弥漫性 WFA 染色强度较低。我们的研究结果表明，HS1 中 PNN 减少、ECM 蛋白改变以及糖基化表达模式的改变可能与耐药性 MTLE 的发病机制和持续存在有关，通过增加 CA 锥体神经元的兴奋性。这项研究证实了 ECM 分子及其调节剂作为耐药性癫痫新治疗方法开发的潜在靶点的有效性。

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