Ku Chia-Chen, Pan Jia-Bin, Wuputra Kenly, Hsu Wen-Li, Kato Kohsuke, Noguchi Michiya, Nakamura Yukio, Saito Shigeo, Tsai Cheng-Yu, Lin Ying-Chu, Wu Deng-Chyang, Lin Chang-Shen, Yokoyama Kazunari K
Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Regenerative Medicine and Cell Therapy Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan.
Cell Death Discov. 2024 Dec 18;10(1):500. doi: 10.1038/s41420-024-02262-2.
The Jun dimerization protein (Jdp2) gene is active in mouse cerebellar granule cells and its protein product plays a crucial role in the formation of the cerebellum lobes through programmed cell death. However, the role of Jdp2 in cellular differentiation and pluripotency in the cerebellum, and the effect of the antioxidation reaction on cell plasticity, remain unknown. N-acetyl-L-cysteine (NAC) induced the early commitment of the differentiation of granule cell precursors (GCPs) to neurons, especially Purkinje cells, via the γ-aminobutyric acid type A receptor α6 subunit (Gabra6) axis; moreover, Jdp2 depletion enhanced this differentiation program of GCPs. The antioxidative effect of NAC was the main driving force of this decision toward the neural differentiation of the GCP population in the presence of Gabra6 in vitro. This implies that antioxidative drugs are effective agents for rescuing oxidative-stress-induced GCP damages in the cerebellum and commit this Gabra6-positive cell population toward differentiation into Purkinje cells.
Jun二聚化蛋白(Jdp2)基因在小鼠小脑颗粒细胞中具有活性,其蛋白质产物通过程序性细胞死亡在小脑叶的形成中起关键作用。然而,Jdp2在小脑细胞分化和多能性中的作用以及抗氧化反应对细胞可塑性的影响仍然未知。N-乙酰-L-半胱氨酸(NAC)通过γ-氨基丁酸A型受体α6亚基(Gabra6)轴诱导颗粒细胞前体(GCPs)向神经元,特别是浦肯野细胞的早期分化;此外,Jdp2的缺失增强了GCPs的这种分化程序。在体外存在Gabra6的情况下,NAC的抗氧化作用是决定GCP群体向神经分化的主要驱动力。这意味着抗氧化药物是挽救小脑氧化应激诱导的GCP损伤并使该Gabra6阳性细胞群体分化为浦肯野细胞的有效药物。