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Peculiarities of the Involvement of MAPKS ERK1/2 and р38 in the Implementation of the Functions of Neural Stem Cells and Neuronal Committed Precursors in Ethanol-Induced Neurodegeneration
Bulletin of Experimental Biology and Medicine ( IF 0.9 ) Pub Date : 2020-09-01 , DOI: 10.1007/s10517-020-04938-y
G N Zyuz'kov 1 , L A Miroshnichenko 1 , T Y Polyakova 1 , L A Stavrova 1 , E V Simanina 1 , V V Zhdanov 1 , A V Chaikovskii 1
Affiliation  

We studied the peculiarities of the participation of ERK1/2 and р38 in regulation of various types of progenitor cells of the nervous tissue under conditions of ethanol-induced neurodegeneration modeled in vitro and in vivo. The stimulating role of these signaling molecules in the realization of the growth potential of intact multipotent neural stem cells and committed neuronal precursors (clonogenic PSA-NCAM+ cells) was demonstrated. In vitro exposure to neurotoxic doses of ethanol led to the loss of the specified role of ERK1/2 and p38 in the cell cycle regulation. Inversion of the role of both studied MAP-kinases in determining the proliferation status of neural stem cells after long-term administration of ethanol to experimental animals was revealed. In committed neuronal precursors, this inversion (inhibition of mitotic activity instead of activation) was revealed only for ERK1/2. In mice exposed to chronic alcoholization, ERK1/2 no longer participated in the process of specialization of both types of regeneration-competent cells of the nerve tissue. The revealed fundamental difference between the functions of ERK1/2 and p38 in the cell cycle regulation in neural stem cells and committed neuronal precursors under optimal conditions and during ethanol-induced neurodegeneration does not allow drawing definite conclusions about the prospect of using modifiers of their activity for the therapy for alcohol-related CNS pathologies.

中文翻译:

MAPKS ERK1/2 和 р38 参与神经干细胞和神经元前体在乙醇诱导的神经变性中的功能的特殊性

我们研究了 ERK1/2 和 р38 在体外和体内建模的乙醇诱导神经变性条件下参与调节神经组织的各种类型祖细胞的特性。证明了这些信号分子在实现完整多能神经干细胞和定向神经元前体(克隆性 PSA-NCAM+ 细胞)的生长潜力方面的刺激作用。体外暴露于神经毒性剂量的乙醇导致 ERK1/2 和 p38 在细胞周期调节中的特定作用丧失。揭示了两种研究的 MAP 激酶在对实验动物长期施用乙醇后确定神经干细胞增殖状态中的作用的倒置。在承诺的神经元前体中,这种反转(抑制有丝分裂活动而不是激活)仅在 ERK1/2 中显示。在暴露于慢性酒精化的小鼠中,ERK1/2 不再参与两种类型的神经组织再生感受态细胞的特化过程。在最佳条件下和乙醇诱导的神经变性期间,ERK1/2 和 p38 在神经干细胞和定向神经元前体的细胞周期调节中的功能之间所揭示的根本差异不允许对使用其活性调节剂的前景得出明确的结论用于治疗酒精相关的中枢神经系统疾病。ERK1/2 不再参与两种类型的神经组织再生感受态细胞的特化过程。在最佳条件下和乙醇诱导的神经变性期间,ERK1/2 和 p38 在神经干细胞和定型神经元前体的细胞周期调节中的功能之间的显着差异不允许对使用其活性调节剂的前景得出明确的结论用于治疗酒精相关的中枢神经系统疾病。ERK1/2 不再参与两种类型的神经组织再生感受态细胞的特化过程。在最佳条件下和乙醇诱导的神经变性期间,ERK1/2 和 p38 在神经干细胞和定型神经元前体的细胞周期调节中的功能之间的显着差异不允许对使用其活性调节剂的前景得出明确的结论用于治疗酒精相关的中枢神经系统疾病。
更新日期:2020-09-01
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