在H2O2诱导的细胞衰老过程中,L1调节蛋白激酶D1 (PKD1) 酸化
Xia Mi1,2,3, Yu Peng1,2, Heng Wu1,2
1The First Affiliated Hospital, Department of Neurology, Multi-Omics Research Center for Brain Disorders, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
L1细胞粘附分子 (L1CAM) 可能抑制氧化应激诱导的衰老. L1CAM上调蛋白激酶D1 (PKD1) 的酸化,提供神经保护,防止细胞衰老.
科学领域:
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 氧化压力有助于与年龄有关的神经退行性疾病.
- L1细胞粘附分子 (L1CAM) 对于神经再生至关重要.
- 蛋白激酶D1 (PKD1) 在神经保护中发挥作用.
研究的目的:
- 调查L1CAM与化PKD1 (pPKD1) 之间的功能联系.
- 确定L1CAM在氧化应激诱导的细胞衰老中的作用.
主要方法:
- 用重组L1 (rL1) 治疗SK-N-SH细胞和人类多能干细胞.
- 在SK-N-SH细胞中使用过氧化 (H2O2) 诱导衰老.
- 评估PKD1酸化,pErk1/2水平,Bcl2/Bax比,以及SA-b-gal阳性细胞.
主要成果:
- rL1上调PKD1酸化,pErk1/2和Bcl2/Bax比率以度依赖的方式.
- 在两种细胞类型中,L1CAM增加了pPKD1水平.
- 在H2O2诱导模型中,L1CAM减少了衰老细胞的数量.
结论:
- L1CAM调节了PKD1的酸化.
- L1CAM在抑制氧化应激诱导的衰老方面表现出潜力.
- 对于与年龄相关的神经退行性疾病,L1CAM可能成为治疗点.
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