Notch 信号通路调控脱髓鞘疾病中 NG2 细胞向少突胶质细胞的分化。
The Notch Signaling Pathway Regulates Differentiation of NG2 Cells into Oligodendrocytes in Demyelinating Diseases.
机构信息
Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, No. 17 Yongwai Zheng Street, Nanchang, 330006, Jiangxi, People's Republic of China.
出版信息
Cell Mol Neurobiol. 2022 Oct;42(7):1-11. doi: 10.1007/s10571-021-01089-0. Epub 2021 Apr 7.
Abstract
NG2 cells are highly proliferative glial cells that can self-renew or differentiate into oligodendrocytes, promoting remyelination. Following demyelination, the proliferative and differentiation potentials of NG2 cells increase rapidly, enhancing their differentiation into functional myelinating cells. Levels of the transcription factors Olig1 and Olig2 increase during the differentiation of NG2 cells and play important roles in the development and repair of oligodendrocytes. However, the ability to generate new oligodendrocytes is hampered by injury-related factors (e.g., myelin fragments, Wnt and Notch signaling components), leading to failed differentiation and maturation of NG2 cells into oligodendrocytes. Here, we review Notch signaling as a negative regulator of oligodendrocyte differentiation and discuss the extracellular ligands, intracellular pathways, and key transcription factors involved.
摘要
NG2 细胞是高度增殖的神经胶质细胞，能够自我更新或分化为少突胶质细胞，促进髓鞘再生。脱髓鞘后，NG2 细胞的增殖和分化潜能迅速增加，促进其分化为具有功能的髓鞘形成细胞。转录因子 Olig1 和 Olig2 的水平在 NG2 细胞的分化过程中增加，在少突胶质细胞的发育和修复中发挥重要作用。然而，新的少突胶质细胞的产生能力受到损伤相关因子（如髓鞘碎片、Wnt 和 Notch 信号成分）的阻碍，导致 NG2 细胞分化为少突胶质细胞的失败和成熟。在这里，我们将 Notch 信号作为少突胶质细胞分化的负调节剂进行综述，并讨论涉及的细胞外配体、细胞内途径和关键转录因子。
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