Endoplasmic Reticulum Stress and the Unfolded Protein Response in Cellular Models of Parkinson's Disease
Open accessAbstract
6-hydroxydopamine, 1-methyl-4-phenyl-pyridinium (MPP+), and rotenone cause the death of dopaminergic neurons in vitro and in vivo and are widely used to model Parkinson's disease. To identify regulated genes in such models, we performed serial analysis of gene expression on neuronal PC12 cells exposed to 6-hydroxydopamine. This revealed a striking increase in transcripts associated with the unfolded protein response. Immunoblotting confirmed phosphorylation of the key endoplasmic reticulum stress kinases IRE1alpha and PERK (PKR-like ER kinase) and induction of their downstream targets. There was a similar response to MPP+ and rotenone, but not to other apoptotic initiators. As evidence that endoplasmic reticulum stress contributes to neuronal death, sympathetic neurons from PERK null mice in which the capacity to respond to endoplasmic reticulum stress is compromised were more sensitive to 6-hydroxydopamine. Our findings, coupled with evidence from familial forms of Parkinson's disease, raise the possibility of widespread involvement of endoplasmic reticulum stress and the unfolded protein response in the pathophysiology of this disease.
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PKR is active in other neurodegenerative diseases, including Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis.
“PKR is not specific to AD because it is also known to be active in other neurodegenerative diseases like Parkinson's disease [49, 170], Huntington's disease [48] and amyotrophic lateral sclerosis [96].”
From PKR, the double stranded RNA‐dependent protein kinase as a critical target in Alzheimer's disease (2009) · cites this paper as [170]
The citation is attached to the Parkinson’s disease portion of the sentence, not the Huntington’s disease or ALS portions. The Abstract and the section ‘ER stress and the UPR are induced by 6-OHDA exposure’ report activation of PERK (PKR-like ER kinase) in Parkinson’s disease models, but do not report activation of PKR. A search for PKR found no passage establishing its activity. (LLM, conf=0.77)
Experimental — accuracy not yet measuredMicroarray analysis of frataxin-deficient mouse heart cells revealed downregulation of the iron-sulfur scaffold protein Isu1, mitochondrial coproporphyrinogen oxidase, and ferrochelatase.
“and microarray analysis of frataxin-deficient mouse heart cells revealed downregulation of the iron-sulfur scaffold protein Isu1, mitochondrial coproporphyrinogen oxidase, and ferrochelatase, which are all involved in the heme pathway (270).”
From Intracellular iron transport and storage: from molecular mechanisms to health implications (2008) · cites this paper as [270]
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- Authors
- Ryu, E. J., Harding, H. P., Angelastro, J. M., Vitolo, O. V., Ron, D., & Greene, L. A.
- Affiliations
- Columbia University Irving Medical Center (US)
- New York University (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2002-12-15
- Volume
- 22
- Issue
- 24
- Pages
- 10690-10698
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6758450
- OpenAlex
- W2152693222
- Cited by
- 572
- References
- 61
- Citations by year
- 2026: 2 · 2025: 10 · 2024: 9 · 2023: 17 · 2022: 16 · 2021: 24 · 2020: 25 · 2019: 19 · 2018: 19 · 2017: 24 · 2016: 25 · 2015: 18 · 2014: 22 · 2013: 25 · 2012: 36
- FWCI
- 8.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Parkinson's Disease Foundation (NS38370)
- National Institutes of Health (NS38370)
- National Institute of Neurological Disorders and Stroke (NS33689, NS160636, NS 436281, P50NS038370, R01NS033689)
- National Institute of Environmental Health Sciences (ES 08681, R01ES008681)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- endoplasmic reticulum stress, unfolded protein response, Parkinson's disease, 6-hydroxydopamine, MPP+, rotenone, dopaminergic neuron death, IRE1α, PERK, PC12 cells, gene expression profiling, neuronal apoptosis
- MeSH terms
- Animals, Cells, Cultured, Dose-Response Relationship, Drug, Endoplasmic Reticulum, Ganglia, Sympathetic, Gene Expression Regulation, Neurons, Parkinson Disease, RNA, Messenger, Rotenone, Sympatholytics, Transcription, Genetic, 1-Methyl-4-phenylpyridinium, Oxidopamine, PC12 Cells, Apoptosis, Protein Folding, Mice, Knockout, eIF-2 Kinase, Gene Expression Profiling, Mice, Rats
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