ACTA VETERINARIA ET ZOOTECHNICA SINICA ›› 2015, Vol. 46 ›› Issue (5): 841-848.doi: 10.11843/j.issn.0366-6964.2015.05.022

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Overexpression of BAT3 Alleviates Prion Protein Fragment PrP106-126-Induced Neuronal Apoptosis

SONG Zhi-qi1# ,ZHAO Wen-jie2# ,YANG Li-feng 1,WANG Yun-sheng 1,ZHU Ting 1,CHENG Guang-yu 1,ZHOU Xiang-mei 1,ZHAO De-ming 1*   

  1. (1.State Key Laboratories for Agrobiotechnology,Key Lab of Animal Epidemiology and Zoonosis,Ministry of Agriculture,National Animal Transmissible Spongiform Encephalopathy Laboratory,College of Veterinary Medicine,China Agricultural University,Beijing 100193,China;2.College of Animal Husbandary and Veterinary Science,Henan Agricultural University,Zhengzhou 450000,China)
  • Received:2014-09-04 Online:2015-05-23 Published:2015-05-23

Abstract:

The objective of this study was to investigate the interactions between BAT3 and prion protein and the potential role of BAT3 in PrP106-126-induced apoptosis.Immunofluorescence,the CCK-8 assay kit and western blotting were used to test the cytotoxicity of PrP106-126-FITC.After the stimulation of PrP106-126-FITC or PrP106-126,the location of BAT3 was tested by immunofluorescence and western blotting in the neurons.BAT3 was overexpressed in Neuro2a or primary neuronal cells by transfection with pcDNA3.1-HA-BAT3 expression plasmids.The effect of BAT3 on PrP106-126-induced cytotoxicity and apoptosis were detected by the CCK-8 assay and TUNEL assay.The expression of cytochrome c and Bcl-2 were examined by western blotting.Results were as follows:PrP106-126-FITC has similar cytotoxicity with PrP106-126.BAT3 interacted with prion protein and enhanced PrP expression.After PrP106-126 peptide treated,BAT3 was transported from the nucleus to cytoplasm,increased cell viability and protected neurons from PrP106-126-induced apoptosis through stabilizing the level of Bcl-2 protein and inhibiting the release of cytochrome c to cytoplasm.Our present data showed a novel molecular mechanism of PrP106-126-induced apoptotic process regulation through the overexpression of BAT3,which may be important for the basic regulatory mechanism of neuron survival in prion diseases and associated neurodegenerative diseases in vivo.

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