Oligodendrocyte precursor cell transplantation promotes angiogenesis and remyelination via Wnt/β-catenin pathway in a mouse model of middle cerebral artery occlusion
Oligodendrocyte precursor cell transplantation promotes angiogenesis and remyelination via Wnt/β-catenin pathway in a mouse model of middle cerebral artery occlusion
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少突胶质细胞前体细胞移植通过 Wnt/β-连环蛋白途径促进大脑中动脉闭塞小鼠模型的血管生成和髓鞘再生
DOI：
10.1177/0271678x211065391
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发表时间：
2021-12-08
影响因子：
6.3
通讯作者：
Yang, Guo-Yuan
中科院分区：
文献类型：
--
作者：
Wang, Li-Ping;Pan, Jiaji;Yang, Guo-Yuan
脑白质损伤是缺血性脑卒中的重要病理特征。少突胶质前体细胞参与缺血性脑损伤脑白质修复和重塑。由于少突胶质前体细胞在中枢神经系统发育过程中可促进wnt依赖性血管生成，沿脉管系统迁移形成髓鞘，我们探讨外源性少突胶质前体细胞移植是否促进小鼠大脑中动脉闭塞后血管生成和髓鞘再生。少突胶质前体细胞移植可改善运动和认知功能，减轻脑萎缩。此外，少突胶质前体细胞移植促进功能性血管生成，并增加缺血性卒中后髓鞘碱性蛋白的表达。进一步研究表明，少突胶质前体细胞移植后的白质修复依赖于Wnt/β-catenin信号通路诱导的血管生成。我们的研究结果表明，来自少突胶质前体细胞的Wnt7a作用于内皮β-连环蛋白，促进血管生成，改善神经行为结果，从而促进缺血性卒中期间白质修复和重塑。
White matter injury is a critical pathological characteristic during ischemic stroke. Oligodendrocyte precursor cells participate in white matter repairing and remodeling during ischemic brain injury. Since oligodendrocyte precursor cells could promote Wnt-dependent angiogenesis and migrate along vasculature for the myelination during the development in the central nervous system, we explore whether exogenous oligodendrocyte precursor cell transplantation promotes angiogenesis and remyelination after middle cerebral artery occlusion in mice. Here, oligodendrocyte precursor cell transplantation improved motor and cognitive function, and alleviated brain atrophy. Furthermore, oligodendrocyte precursor cell transplantation promoted functional angiogenesis, and increased myelin basic protein expression after ischemic stroke. The further study suggested that white matter repairing after oligodendrocyte precursor cell transplantation depended on angiogenesis induced by Wnt/β-catenin signal pathway. Our results demonstrated a novel pathway that Wnt7a from oligodendrocyte precursor cells acting on endothelial β-catenin promoted angiogenesis and improved neurobehavioral outcomes, which facilitated white matter repair and remodeling during ischemic stroke.