JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2015, Vol. 53 ›› Issue (10): 1-5.doi: 10.6040/j.issn.1671-7554.0.2014.684

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Mechanism of mitophagy in a cell model of Alzheimer's disease

ZHAO Xuelian1, YU Jun2, XIE Zhaohong1, CAO Yanjun1, LIU Zhen1, WANG Xiao1, XU Linlin1, YANG Hui1, ZHENG Xiaolei1, SHEN Yang1, BI Jianzhong1   

  1. 1. Department of Neurology, the Second Hospital of Shandong University, Jinan 250033, Shandong, China;
    2. The Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250011, Shandong, China
  • Received:2014-10-10 Online:2015-10-10 Published:2015-10-10

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Abstract: Objective To investigate the effect of autophagy involved in Alzheimer's disease cell model 20E2 and its possible mechanism. Methods To determine whether the 20E2 cells model was successfully established, we detected the levels of Aβ1-40 in HEK293 cells and 20E2 cells (HEK293 cells stably expressing Swedish mutant APP) cultured in vitro by ELISA kit, and the expression of APP protein level was detected by Western blotting. The mitochondria in cells was observed by electron microscope. The mitochondrial membrane potential of both cells was detected by fluorescence probe JC-1. Flow cytometry was used to measure the apoptotic rate. LC3-II, PINK1 and Parkin were detected by Western blotting. Results The expression levels of APP protein and Aβ1-40 increased in 20E2 cells compared with those in HEK293 cells. Mitochondrial swollen, cristae disappeared and vacuolization was obviously observed. Mitochondrial membrane potential decreased. The expression levels of PINK1, Parkin and LC3-II increased (P<0.05). Conclusion In Alzheimer's disease cell model 20E2, the mitochondrial morphology changed obviously and membrane potential of mitochondria declined, and these changes may cause the increase of mitochondrial autophagy through PINK1 and Parkin pathway.

Key words: Mitochondrial membrane potential, Parkin, Alzheimer's disease, PINK1, Mitophagy

CLC Number: 

  • R741.02
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