Soluble factor effects on glial cell reactivity at the surface of gel-coated microwires.
Soluble factor effects on glial cell reactivity at the surface of gel-coated microwires.
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DOI：
10.1016/j.jneumeth.2010.05.002
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发表时间：
2010-07-15
影响因子：
3
通讯作者：
Reichert, William M.
中科院分区：
文献类型：
--
作者：
Polikov, Vadim S.;Hong, Jau-Shyong;Reichert, William M.
关键词：
将基底层凝胶制剂纳入改良的神经炎症细胞培养模型中，以测试该系统作为表面改性微丝的表征工具。凝胶涂层微丝表面的神经胶质增生程度是通过用许多据报道参与反应性神经胶质增生的可溶性因子滴定细胞培养物来定量的。阳性对照条件（1% FBS、10ng/ml bFGF、添加 B27 的神经基础培养基）诱导一层表达 GFAP 的星形胶质细胞在所有凝胶涂层微线上积聚。血清、炎性细胞因子 IL-1α 和 IL-1β 以及神经祖细胞 (NPC) 增殖生长因子 bFGF 和 PDGF 均增加了凝胶上反应细胞的数量，这与报道的它们在损伤部位细胞活化、迁移和增殖中的作用一致。从技术上讲，这项研究表明，胎儿神经元-胶质细胞培养系统非常适合表征旨在减轻植入物相关神经胶质增生的电极涂层的影响，以及筛选促进和/或抑制植入物相关神经胶质增生的多种可溶性因子的影响。从科学角度来看，这项研究指出了血清和炎症因子在诱导 NPC 激活和迁移至损伤部位方面的重要作用，其中 bFGF 和 PDGF 等生长因子诱导细胞增殖，最终形成神经胶质疤痕。
A basal lamina gel preparation was incorporated into a modified neuroinflammation cell culture model to test the system as a characterization tool for surface-modified microwires. The extent of gliosis at the surface of gel-coated microwires was quantified in response to titrating the cell culture with a number of soluble factors reported to be involved in reactive gliosis. Positive control conditions (1% FBS, 10ng/ml bFGF, Neural Basal medium with B27 supplement) induced a layer of GFAP-expressing astrocytes to accumulate on all gel-coated microwires. Serum, inflammatory cytokines IL-1α and IL-1β and the neural progenitor cell (NPC) proliferating growth factors bFGF and PDGF all increased the number of reactive cells on the gel, in agreement with their reported roles in cell activation, migration and proliferation at the site of injury. Technically, this study shows that a fetal neuron-glia culture system is well suited for characterizing the impact of electrode coatings designed to mitigate implant-associated gliosis, and for screening the effect of multiple soluble factors that promote and/or inhibit implant-associated gliosis. Scientifically, this study points to essential roles of serum and inflammatory factors to induce NPC activation and migration to the site of injury, where growth factors like bFGF and PDGF induce proliferation of cells that will eventually form the glial scar.
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