Hospital Nacional de Parapléjicos, Servicio de Salud de Castilla La Mancha, 45071 Toledo, Spain.
Departamento de Química Bio-Orgánica, Instituto de Química Orgánica General (IQOG-CSIC), CSIC, 28006 Madrid, Spain.
Int J Mol Sci. 2024 Aug 23;25(17):9173. doi: 10.3390/ijms25179173.
Traumatic spinal cord injury (tSCI) has complex pathophysiological events that begin after the initial trauma. One such event is fibroglial scar formation by fibroblasts and reactive astrocytes. A strong inhibition of axonal growth is caused by the activated astroglial cells as a component of fibroglial scarring through the production of inhibitory molecules, such as chondroitin sulfate proteoglycans or myelin-associated proteins. Here, we used neural precursor cells (aldynoglia) as promoters of axonal growth and a fibrin hydrogel gelled under alkaline conditions to support and guide neuronal cell growth, respectively. We added Tol-51 sulfoglycolipid as a synthetic inhibitor of astrocyte and microglia in order to test its effect on the axonal growth-promoting function of aldynoglia precursor cells. We obtained an increase in GFAP expression corresponding to the expected glial phenotype for aldynoglia cells cultured in alkaline fibrin. In co-cultures of dorsal root ganglia (DRG) and aldynoglia, the axonal growth promotion of DRG neurons by aldynoglia was not affected. We observed that the neural precursor cells first clustered together and then formed niches from which aldynoglia cells grew and connected to groups of adjacent cells. We conclude that the combination of alkaline fibrin with synthetic sulfoglycolipid Tol-51 increased cell adhesion, cell migration, fasciculation, and axonal growth capacity, promoted by aldynoglia cells. There was no negative effect on the behavior of aldynoglia cells after the addition of sulfoglycolipid Tol-51, suggesting that a combination of aldynoglia plus alkaline fibrin and Tol-51 compound could be useful as a therapeutic strategy for tSCI repair.
创伤性脊髓损伤(tSCI)有复杂的病理生理事件,始于初始创伤后。其中一个事件是成纤维细胞和反应性星形胶质细胞形成纤维胶质瘢痕。活化的星形胶质细胞通过产生抑制分子,如硫酸软骨素蛋白聚糖或髓鞘相关蛋白,作为纤维胶质瘢痕形成的一部分,强烈抑制轴突生长。在这里,我们使用神经前体细胞(aldynoglia)作为轴突生长的促进剂,并使用在碱性条件下凝胶化的纤维蛋白水凝胶分别支持和引导神经元细胞生长。我们添加 Tol-51 硫酸糖脂作为星形胶质细胞和小胶质细胞的合成抑制剂,以测试其对 aldynoglia 前体细胞的促轴突生长功能的影响。我们获得了与 aldynoglia 细胞在碱性纤维蛋白中培养时预期的神经胶质表型相对应的 GFAP 表达增加。在背根神经节(DRG)和 aldynoglia 的共培养物中,aldynoglia 对 DRG 神经元的轴突生长促进作用不受影响。我们观察到神经前体细胞首先聚集在一起,然后形成由 aldynoglia 细胞生长并连接到相邻细胞群的小生境。我们得出结论,碱性纤维蛋白与合成硫酸糖脂 Tol-51 的组合增加了 aldynoglia 细胞的细胞黏附、细胞迁移、成束和轴突生长能力。添加 Tol-51 硫酸糖脂后,aldynoglia 细胞的行为没有负面影响,这表明 aldynoglia 加碱性纤维蛋白和 Tol-51 化合物的组合可能是治疗 tSCI 修复的有效策略。