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Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans
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Glycosylation modification of human prion protein provokes apoptosis in HeLa cells in vitro

Yang Yang1, Lan Chen, Hua-Zhen Pan

  • 1National Laboratory of Medical Molecular Biology, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Science, Chinese Academy of Medical Sciences, Beijing 100005, People's Republic of China. caiminxu@yahoo.com.cn

BMB Reports
|June 30, 2009
PubMed

Insights

Non-glycosylated prion proteins (PrP) trigger cell death through apoptosis. This occurs via the mitochondria-mediated pathway, involving reactive oxygen species and altered apoptosis-related protein levels.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Prion diseases are linked to misfolded prion proteins (PrP).
  • The role of PrP glycosylation in cellular processes like apoptosis is not fully understood.

Purpose of the Study:

  • To investigate the correlation between glycosylation-modified prion proteins and apoptosis.
  • To elucidate the cellular mechanisms underlying PrP-induced apoptosis.

Main Methods:

  • Transient expression of wild-type and mutant PRNP genes in HeLa cells.
  • Apoptosis assessment using MTT assay, Hochest, Annexin-V, and PI staining.
  • Analysis of reactive oxygen species (ROS) generation, mitochondrial membrane potential, and key apoptosis-related proteins (Bcl-xL, Bax, cleaved Caspase-9) via Western Blot and flow cytometry.

Main Results:

  • Non-glycosylated PrP significantly induced apoptosis and inhibited cell growth.
  • Expressed non-glycosylated PrP led to reduced mitochondrial membrane potential and increased ROS generation.
  • Downregulation of Bcl-xL and upregulation of cleaved Caspase-9 were observed in response to non-glycosylated PrP.

Conclusions:

  • Non-glycosylated PrP induces apoptosis in HeLa cells.
  • The mechanism of apoptosis induced by non-glycosylated PrP involves the mitochondria-mediated signal transduction pathway.

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