A spatiotemporal study of gliosis in relation to depth electrode tracks in drug-resistant epilepsy.
A spatiotemporal study of gliosis in relation to depth electrode tracks in drug-resistant epilepsy.
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DOI：
10.1111/ejn.12548
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发表时间：
2014-06
期刊：
影响因子：
--
通讯作者：
Thom M
中科院分区：
文献类型：
--
作者：
Goc J;Liu JY;Sisodiya SM;Thom M
关键问题仍然是关于中枢神经系统损伤后神经胶质细胞生成的过程，这对于理解有益的脑修复机制和任何长期的有害影响（包括癫痫发作风险增加）至关重要。我们使用颅内电极（ICE）产生的皮质损伤来研究手术切除的人脑组织中神经胶质增生和神经胶质生成的时间过程和定位。选择17例4-301天的ICE损伤病例。使用增殖细胞标记物（MCM 2）、命运特异性转录因子标记物（PAX 6、SOX 2）、小胶质细胞标记物（IBA 1）和胶质细胞标记物（巢蛋白、GFAP）在三个区域进行双标记免疫标记定量：与ICE损伤部位相关的1区（紧邻：0-350 μm）、2区（350-700 μm）和3区（远端≥2000 μm）。小胶质细胞/巨噬细胞密度在损伤后（dpi）28-30天达到峰值，在所有区域中增殖的小胶质细胞随着dpi显著下降。巢蛋白表达细胞（NEC）集中在1区和2区，显示出最高的再生能力（MCM 2和PAX 6共表达），并与组织损伤腔内的毛细血管密切相关。在区域1和2中，nestin/MCM 2共表达细胞随着dpi显著下降。巢蛋白阳性纤维仍在慢性疤痕，和神经元形态的NEC指出，在旧的损伤。表达GFAP的神经胶质细胞更均匀地分布在区域之间，密度或增殖能力随着dpi没有显著下降。1区胶质细胞中nestin和GFAP的共定位随着DPI的增加而减少。总之，在急性损伤部位的神经内皮细胞是一个增殖的，短暂的细胞群，具有成熟为星形胶质细胞的能力，在老年损伤中观察到可能的神经元分化。
Key questions remain regarding the processes governing gliogenesis following central nervous system injury that are critical to understanding both beneficial brain repair mechanisms and any long-term detrimental effects, including increased risk of seizures. We have used cortical injury produced by intracranial electrodes (ICEs) to study the time-course and localization of gliosis and gliogenesis in surgically resected human brain tissue. Seventeen cases with ICE injuries of 4–301 days age were selected. Double-labelled immunolabelling using a proliferative cell marker (MCM2), markers of fate-specific transcriptional factors (PAX6, SOX2), a microglial marker (IBA1) and glial markers (nestin, GFAP) was quantified in three regions: zone 1 (immediate vicinity: 0–350 μm), zone 2 (350–700 μm) and zone 3 (remote ≥2000 μm) in relation to the ICE injury site. Microglial/macrophage cell densities peaked at 28–30 days post-injury (dpi) with a significant decline in proliferating microglia with dpi in all zones. Nestin-expressing cells (NECs) were concentrated in zones 1 and 2, showed the highest regenerative capacity (MCM2 and PAX6 co-expression) and were intimately associated with capillaries within the organizing injury cavity. There was a significant decline in nestin/MCM2 co-expressing cells with dpi in zones 1 and 2. Nestin-positive fibres remained in the chronic scar, and NECs with neuronal morphology were noted in older injuries. GFAP-expressing glia were more evenly distributed between zones, with no significant decline in density or proliferative capacity with dpi. Colocalization between nestin and GFAP in zone 1 glial cells decreased with increasing dpi. In conclusion, NECs at acute injury sites are a proliferative, transient cell population with capacity for maturation into astrocytes with possible neuronal differentiation observed in older injuries.
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DOI：
10.1523/jneurosci.4707-08.2009
发表时间：
2009-03-11
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Oberheim NA;Takano T;Han X;He W;Lin JH;Wang F;Xu Q;Wyatt JD;Pilcher W;Ojemann JG;Ransom BR;Goldman SA;Nedergaard M
通讯作者：
Nedergaard M
影响因子：
5.1
作者：
Kang, Wenfei;Hebert, Jean M.
通讯作者：
Hebert, Jean M.
影响因子：
5
作者：
Moreels, M.;Vandenabeele, F.;Lambrichts, I.
通讯作者：
Lambrichts, I.
影响因子：
6.2
作者：
Baumgart, Emily Violette;Barbosa, Joana S.;Ninkovic, Jovica
通讯作者：
Ninkovic, Jovica
影响因子：
3.6
作者：
Shin, Yoo-Jin;Kim, Hong Lim;Lee, Mun-Yong
通讯作者：
Lee, Mun-Yong