ArticleFree radical biology & medicine2008
Opposing roles of prion protein in oxidative stress- and ER stress-induced apoptotic signaling.
Article in Free radical biology & medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Cellular prion protein offers neuroprotection in astrocytes submitted to amyloid β oligomer toxicity.Molecular and cellular biochemistry · 2023Article
- The Cellular Prion Protein: A Promising Therapeutic Target for Cancer.International journal of molecular sciences · 2020Review
- An Ex Vivo Brain Slice Culture Model of Chronic Wasting Disease: Implications for Disease Pathogenesis and Therapeutic Development.Scientific reports · 2020Article
- Protective effects of selenium against zearalenone-induced apoptosis in chicken spleen lymphocyte via an endoplasmic reticulum stress signaling pathway.Cell stress & chaperones · 2019Article
- Article
- Integrated Organotypic Slice Cultures and RT-QuIC (OSCAR) Assay: Implications for Translational Discovery in Protein Misfolding Diseases.Scientific reports · 2017Article
- Physiological Functions of the Cellular Prion Protein.Frontiers in molecular biosciences · 2017Review
- Article
- Hypoxia-induced expression of cellular prion protein improves the therapeutic potential of mesenchymal stem cells.Cell death & disease · 2016Article
- Creutzfeldt-Jakob Disease Subtype-Specific Regional and Temporal Regulation of ADP Ribosylation Factor-1-Dependent Rho/MLC Pathway at Pre-Clinical Stage.Journal of molecular neuroscience : MN · 2015Article
- Article
- Up-regulation of mRNA ventricular PRNP prion protein gene expression in air pollution highly exposed young urbanites: endoplasmic reticulum stress, glucose regulated protein 78, and nanosized particles.International journal of molecular sciences · 2013Article
- Effect of divalent metals on the neuronal proteasomal system, prion protein ubiquitination and aggregation.Toxicology letters · 2012Article
- Silencing prion protein in MDA-MB-435 breast cancer cells leads to pleiotropic cellular responses to cytotoxic stimuli.PloS one · 2012Article
- Recruitment of cellular prion protein to mitochondrial raft-like microdomains contributes to apoptosis execution.Molecular biology of the cell · 2011Article
- Infectious prion protein alters manganese transport and neurotoxicity in a cell culture model of prion disease.Neurotoxicology · 2011Article
- Neuroprotective role of PrPC against kainate-induced epileptic seizures and cell death depends on the modulation of JNK3 activation by GluR6/7-PSD-95 binding.Molecular biology of the cell · 2011Article
- Review
- The fatal attraction between pro-prion and filamin A: prion as a marker in human cancers.Biomarkers in medicine · 2010Article
- Manganese upregulates cellular prion protein and contributes to altered stabilization and proteolysis: relevance to role of metals in pathogenesis of prion disease.Toxicological sciences : an official journal of the Society of Toxicology · 2010Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Although the prion protein is abundantly expressed in the CNS, its biological functions remain unclear. To determine the endogenous function of the cellular prion protein (PrP(c)), we compared the effects of oxidative stress and endoplasmic reticulum (ER) stress inducers on apoptotic signaling in PrP(c)-expressing and PrP(ko) (knockout) neural cells. H(2)O(2), brefeldin A (BFA), and tunicamycin (TUN) induced increases in caspase-9 and caspase-3, PKCdelta proteolytic activation, and DNA fragmentation in PrP(c) and PrP(ko) cells. Interestingly, ER stress-induced activation of caspases, PKCdelta, and apoptosis was significantly exacerbated in PrP(c) cells, whereas H(2)O(2)-induced proapoptotic changes were suppressed in PrP(c) compared to PrP(ko) cells. Additionally, caspase-12 and caspase-8 were activated only in the BFA and TUN treatments. Inhibitors of caspase-9, caspase-3, and PKCdelta significantly blocked H(2)O(2)-, BFA-, and TUN-induced apoptosis, whereas the caspase-8 inhibitor attenuated only BFA- and TUN-induced cell death, and the antioxidant MnTBAP blocked only H(2)O(2)-induced apoptosis. Overexpression of the kinase-inactive PKCdelta(K376R) or the cleavage site-resistant PKCdelta(D327A) mutant suppressed both ER and oxidative stress-induced apoptosis. Thus, PrP(c) plays a proapoptotic role during ER stress and an antiapoptotic role during oxidative stress-induced cell death. Together, these results suggest that cellular PrP enhances the susceptibility of neural cells to impairment of protein processing and trafficking, but decreases the vulnerability to oxidative insults, and that PKCdelta is a key downstream mediator of cellular stress-induced neuronal apoptosis.
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Registered trials
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