The involvement of cellular prion protein in the autophagy pathway in neuronal cells

Oxidative stress impairs autophagic flux in prion protein-deficient hippocampal cells

“…Prnp +/+ and Prnp 0/0 cell lines were previously established as described in ref. 36. All cell lines were cultivated in DMEM supplemented with 10% FBS and 1% penicillin-streptomycin in a 5% CO 2 atmosphere at 37°C.…”

“…This increased autophagy is suppressed in Prnp 0/0 cells transfected with the Prnp gene. 36 However, it is unclear whether increased autophagy contributes to the activation of cell survival or cell death pathways. In transformed and cancer cell lines, oxidative stress-induced autophagic cell death persisted upon treatment with reactive oxygen species (ROS)-generating agents, such as hydrogen peroxide (H 2 O 2 ) and 2-methoxyestradiol.…”

“…38,39 To investigate further a mechanism for the protective role of PrP C in oxidative stress, we examined the alteration and differentiation of autophagy under H 2 O 2 -induced oxidative stress in hippocampal neuronal cell lines expressing PrP C (Prnp +/+ ) and a control vector (Prnp 0/0 ). 36,40 In addition, we explored whether the inhibition or induction of autophagy could promote cell survival or cell death. In these experiments, we show that the expression of the autophagy marker LC3B-II was more increased in (Fig.…”

Autophagy, Prion Infection and their Mutual Interactions

“…An increased expression of LC3-II was observed in hippocampal neurons of Zürich I Prnp -/-mice as compared to wild-type control neurons under serum deprivation and this up-regulation was counter-acted by reintroduction of PrP c into Prnp -/-cells (Oh et al, 2008). As such counter-regulation was not detectable for PrP c lacking the octapeptide region, it was suggested that the octapeptide region of PrP c may play a crucial role in control of autophagy in neuronal cells as mediated by PrP c .…”

Investigation of the role of prion protein in protection against transition metal induced toxicity

“…Zpl 2-1 has been shown to be more vulnerable to serum deprivation and oxidative damage induced by H 2 O 2 than its PrP-expressing counterpart (Kim et al, 2004;Oh et al, 2008Oh et al, , 2012. Reintroduction of PrP restored the viability of Zpl cells, thus, it seems to be a relevant model for assessing the effect of PrP C on metal-induced toxicity as well.…”