β-淀粉样蛋白诱导神经退行性变条件下 MARK ERK1/2 和 p38 在神经干细胞和神经胶质细胞功能调节中的作用。
The Role of MARK ERK1/2 and p38 in Regulation of Functions of Neural Stem Cells and Neuroglia under Conditions of β-Amyloid-Induced Neurodegeneration.
机构信息
E. D. Goldberg Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
出版信息
Bull Exp Biol Med. 2022 Aug;173(4):424-428. doi: 10.1007/s10517-022-05561-9. Epub 2022 Sep 5.
Abstract
The role of ERK1/2 and p38 in the realization of the growth potential of neural stem cells and secretion of neurotrophic growth factors by glial cells was studied using in vitro model of β-amyloid-induced neurodegeneration. It was shown that amyloid-β fragment 25-35 significantly inhibits the cell cycle progression of neural stem cells against the background of stimulation of their differentiation and reduced production of growth factors by neuroglia. The inhibitory role of ERK1/2 and p38 in relation to the proliferative activity of neural stem cells and the secretory activity of glial elements was revealed. ERK1/2 and p38 inhibitors increased proliferation of progenitor cells of the nervous tissue and reduced the intensity of their specialization, as well as stimulated production of growth factors by neuroglial cells under conditions of simulated β-amyloid-induced neurodegeneration.
摘要
采用β-淀粉样蛋白诱导神经退行性变的体外模型研究了 ERK1/2 和 p38 在神经干细胞生长潜能的实现和神经胶质细胞分泌神经营养生长因子中的作用。结果表明，淀粉样β片段 25-35 显著抑制神经干细胞的细胞周期进程，同时刺激其分化，并减少神经胶质细胞生长因子的产生。揭示了 ERK1/2 和 p38 与神经干细胞增殖活性和神经胶质细胞分泌活性的抑制作用。ERK1/2 和 p38 抑制剂在模拟β-淀粉样蛋白诱导的神经退行性变条件下增加了神经组织祖细胞的增殖，降低了其特化程度，并刺激了神经胶质细胞生长因子的产生。
相似文献
1
The Role of MARK ERK1/2 and p38 in Regulation of Functions of Neural Stem Cells and Neuroglia under Conditions of β-Amyloid-Induced Neurodegeneration.β-淀粉样蛋白诱导神经退行性变条件下 MARK ERK1/2 和 p38 在神经干细胞和神经胶质细胞功能调节中的作用。
Bull Exp Biol Med. 2022 Aug;173(4):424-428. doi: 10.1007/s10517-022-05561-9. Epub 2022 Sep 5.
2
The Role of JAKs and STAT3 in Regulation of Regenerative-Competent Cells of the Nervous Tissue in β-Amyloid-Induced Neurodegeneration.JAKs 和 STAT3 在β-淀粉样蛋白诱导的神经变性中对神经组织再生能力细胞的调控作用。
Bull Exp Biol Med. 2022 Aug;173(4):419-423. doi: 10.1007/s10517-022-05560-w. Epub 2022 Sep 5.
3
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.乙醇诱导神经退行性变中 MAPKs ERK1/2 和 р38 参与神经干细胞和神经定向前体细胞功能的特点。
Bull Exp Biol Med. 2020 Sep;169(5):609-613. doi: 10.1007/s10517-020-04938-y. Epub 2020 Sep 26.
4
Role of MAPK ERK1/2 and p38 in the Realization of Growth Potential of Various Types of Regeneration-Competent Cells in Mouse Neural Tissue during Ethanol-Induced Neurodegeneration In Vitro.丝裂原活化蛋白激酶ERK1/2和p38在乙醇诱导的体外小鼠神经组织各种具有再生能力的细胞生长潜能实现中的作用
Bull Exp Biol Med. 2019 Jun;167(2):229-232. doi: 10.1007/s10517-019-04497-x. Epub 2019 Jun 24.
5
Role of MAPK ERK1/2 and p38 in the Regulation of Secretory Functions of Different Populations of Neuroglia in Ethanol-Induced Neurodegeneration.丝裂原活化蛋白激酶ERK1/2和p38在乙醇诱导的神经退行性变中不同神经胶质细胞群分泌功能调节中的作用
Bull Exp Biol Med. 2021 Oct;171(6):699-703. doi: 10.1007/s10517-021-05298-x. Epub 2021 Oct 28.
6
Functional State of Various Types of Regenerative-Competent Neural Tissue Cells in β-Amyloid-Induced Neurodegeneration.β-淀粉样蛋白诱导的神经退行性变中各种类型再生能力神经组织细胞的功能状态。
Bull Exp Biol Med. 2022 Oct;173(6):709-713. doi: 10.1007/s10517-022-05617-w. Epub 2022 Nov 2.
7
The Role of JNK and p53 in the Regulation of Secretory Function of Neuroglial Cells of Various Types in β-Amyloid-Induced Neurodegeneration.JNK 和 p53 在β-淀粉样蛋白诱导的神经退行性变中各种类型神经胶质细胞分泌功能调节中的作用。
Bull Exp Biol Med. 2023 Oct;175(6):753-756. doi: 10.1007/s10517-023-05939-3. Epub 2023 Nov 21.
8
The Role of Smad3 in the Realization of the Growth Potential of Different Types of Neural Progenitor Cells and the Secretory Function of Neuroglia.Smad3 在不同类型神经祖细胞生长潜能实现和神经胶质细胞分泌功能中的作用。
Bull Exp Biol Med. 2024 May;177(1):35-38. doi: 10.1007/s10517-024-06126-8. Epub 2024 Jul 2.
9
ERK1/2 and p38 MAP kinases control prion protein fragment 90-231-induced astrocyte proliferation and microglia activation.细胞外信号调节激酶1/2（ERK1/2）和p38丝裂原活化蛋白激酶（p38 MAPK）调控朊病毒蛋白片段90 - 231诱导的星形胶质细胞增殖和小胶质细胞活化。
Glia. 2007 Nov 1;55(14):1469-85. doi: 10.1002/glia.20559.
10
Amyloid-β dynamically regulates the migration of neural stem/progenitor cells via MAPK-ERK pathway.淀粉样蛋白-β 通过 MAPK-ERK 通路动态调节神经干细胞/祖细胞的迁移。
Chem Biol Interact. 2019 Jan 25;298:96-103. doi: 10.1016/j.cbi.2018.11.001. Epub 2018 Nov 3.
引用本文的文献
1
Apatinib Mesylate Inhibits Cell Proliferation and the Metastasis of Esophageal Squamous Cell Carcinoma Through ERK/ELK-1/Snail Pathway.甲磺酸阿帕替尼通过ERK/ELK-1/Snail通路抑制食管鳞状细胞癌的细胞增殖和转移。
Cell Biochem Biophys. 2025 Jun;83(2):2201-2211. doi: 10.1007/s12013-024-01631-z. Epub 2024 Dec 21.
2
Targeting Adenylate Cyclase: A Novel Concept for Stimulation of Neurogenesis and Pharmacotherapy of Alzheimer's Disease.靶向腺苷酸环化酶：刺激神经发生及阿尔茨海默病药物治疗的新概念
Cent Nerv Syst Agents Med Chem. 2025;25(2):169-180. doi: 10.2174/0118715249302264240715060630.
本文引用的文献
1
A case of xenon inhalation therapy for respiratory failure and neuropsychiatric disorders associated with COVID-19.1例新冠病毒肺炎相关呼吸衰竭及神经精神障碍的氙气吸入治疗病例。
EXCLI J. 2021 Oct 28;20:1517-1525. doi: 10.17179/excli2021-4316. eCollection 2021.
2
Role of MAPK ERK1/2 and p38 in the Regulation of Secretory Functions of Different Populations of Neuroglia in Ethanol-Induced Neurodegeneration.丝裂原活化蛋白激酶ERK1/2和p38在乙醇诱导的神经退行性变中不同神经胶质细胞群分泌功能调节中的作用
Bull Exp Biol Med. 2021 Oct;171(6):699-703. doi: 10.1007/s10517-021-05298-x. Epub 2021 Oct 28.
3
Targeting cAMP-pathway in Regeneration-competent Cells of Nervous Tissue: Potential to Create a Novel Drug for Treatment of Ethanol-induced Neurodegeneration.靶向神经组织中具有再生能力的细胞中的 cAMP 通路：开发新型药物治疗乙醇诱导的神经退行性变的潜力。
Cent Nerv Syst Agents Med Chem. 2021;21(3):172-180. doi: 10.2174/1871524921666210907102847.
4
Specific Features of Intracellular Signal Transduction in the Regulation of Functions of Neural Stem Cells and Committed Neuronal Progenitors.神经干细胞和定向分化神经元前体细胞功能调控的细胞内信号转导的特定特征。
Bull Exp Biol Med. 2021 Feb;170(4):522-527. doi: 10.1007/s10517-021-05100-y. Epub 2021 Mar 16.
5
Stem Cell Therapy for Alzheimer's Disease.干细胞治疗阿尔茨海默病。
Adv Exp Med Biol. 2020;1266:39-55. doi: 10.1007/978-981-15-4370-8_4.
6
Alzheimer's disease: Recent treatment strategies.阿尔茨海默病：近期治疗策略
Eur J Pharmacol. 2020 Nov 15;887:173554. doi: 10.1016/j.ejphar.2020.173554. Epub 2020 Sep 15.
7
Neuro-inflammation and anti-inflammatory treatment options for Alzheimer's disease.神经炎症与阿尔茨海默病的抗炎治疗选择。
Clin Biochem. 2019 Oct;72:87-89. doi: 10.1016/j.clinbiochem.2019.04.001. Epub 2019 Apr 4.
8
Somatic APP gene recombination in Alzheimer's disease and normal neurons.阿尔茨海默病和正常神经元中的体细胞 APP 基因重组。
Nature. 2018 Nov;563(7733):639-645. doi: 10.1038/s41586-018-0718-6. Epub 2018 Nov 21.
9
Amyloid-β dynamically regulates the migration of neural stem/progenitor cells via MAPK-ERK pathway.淀粉样蛋白-β 通过 MAPK-ERK 通路动态调节神经干细胞/祖细胞的迁移。
Chem Biol Interact. 2019 Jan 25;298:96-103. doi: 10.1016/j.cbi.2018.11.001. Epub 2018 Nov 3.
10
Neuronal and Glial Differentiation of Human Neural Stem Cells Is Regulated by Amyloid Precursor Protein (APP) Levels.人神经干细胞的神经元和神经胶质分化受淀粉样前体蛋白（APP）水平的调节。
Mol Neurobiol. 2019 Feb;56(2):1248-1261. doi: 10.1007/s12035-018-1167-9. Epub 2018 Jun 7.
Zotero 插件