ArticleNeuromolecular medicine2008
Coupling endoplasmic reticulum stress to the cell death program in dopaminergic cells: effect of paraquat.
Article in Neuromolecular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 56 citations in OpenAlex.
- Strategies targeting endoplasmic reticulum stress to improve Parkinson's disease.Frontiers in pharmacology · 2023Review
- Curcumin supplementation increases longevity and antioxidant capacity inFrontiers in pharmacology · 2023Article
- Selenium Effects on Oxidative Stress-Induced Calcium Signaling Pathways in Parkinson's Disease.Indian journal of clinical biochemistry : IJCB · 2022Review
- Cellular and Molecular Events Leading to Paraquat-Induced Apoptosis: Mechanistic Insights into Parkinson's Disease Pathophysiology.Molecular neurobiology · 2022Review
- Article
- Review
- Toxicant-mediated redox control of proteostasis in neurodegeneration.Current opinion in toxicology · 2019Article
- Hsp90 Co-chaperone p23 contributes to dopaminergic mitochondrial stress via stabilization of PHD2: Implications for Parkinson's disease.Neurotoxicology · 2018Article
- Cellular Senescence Is Induced by the Environmental Neurotoxin Paraquat and Contributes to Neuropathology Linked to Parkinson's Disease.Cell reports · 2018Article
- The Role of IRE1 Signaling in the Central Nervous System Diseases.Current neuropharmacology · 2018Review
- Overexpression of p58ipk protects neuroblastoma against paraquat-induced toxicity.International journal of clinical and experimental pathology · 2017Article
- A high content screening approach to identify molecules neuroprotective for photoreceptor cells.Advances in experimental medicine and biology · 2014Article
- High-throughput screening identifies aclacinomycin as a radiosensitizer of EGFR-mutant non-small cell lung cancer.Translational oncology · 2013Article
- The unfolded protein response triggered by environmental factors.Seminars in immunopathology · 2013Review
- The small co-chaperone p23 overexpressing transgenic mouse.Journal of neuroscience methods · 2013Article
- Ceramide sphingolipid signaling mediates Tumor Necrosis Factor (TNF)-dependent toxicity via caspase signaling in dopaminergic neurons.Molecular neurodegeneration · 2012Article
- The small chaperone protein p23 and its cleaved product p19 in cellular stress.Journal of molecular neuroscience : MN · 2012Article
- A possible novel anti-inflammatory mechanism for the pharmacological prolyl hydroxylase inhibitor 3,4-dihydroxybenzoate: implications for use as a therapeutic for Parkinson's disease.Parkinson's disease · 2012Article
- Differential regional expression patterns of α-synuclein, TNF-α, and IL-1β; and variable status of dopaminergic neurotoxicity in mouse brain after Paraquat treatment.Journal of neuroinflammation · 2011Article
- The endoplasmic reticulum-associated degradation is necessary for plant salt tolerance.Cell research · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Parkinson's disease (PD) features oxidative stress and accumulation of misfolded (unfolded, alternatively folded, or mutant) proteins with associated loss of dopaminergic neurons. Oxidative stress and the accumulated misfolded proteins elicit cellular responses that include an endoplasmic reticulum (ER) stress response that may protect cells against the toxic buildup of misfolded proteins. Chronic ER stress and accumulation of misfolded proteins in excessive amounts, however, overwhelm the cellular 'quality control' system and impair the protective mechanisms designed to promote correct folding and degrade faulty proteins, ultimately leading to organelle dysfunction and neuronal cell death. Paraquat belongs to a class of bipyridyl herbicides and triggers oxidative stress and dopaminergic cell death. Epidemiological studies suggest an increased risk for developing PD following chronic exposure to paraquat. The present study was carried out to determine the role of paraquat in triggering cellular stress particularly ER stress and to elucidate the pathways that couple ER stress to dopaminergic cell death. We demonstrate that paraquat triggers ER stress, cell dysfunction, and dopaminergic cell death. p23, a small co-chaperone protein, is cleaved during ER stress-induced cell death triggered by paraquat and blockage of the caspase cleavage site of p23 was associated with decreased cell death. Paraquat also inhibits proteasomal activity that may further trigger accumulation of misfolded proteins resulting in ER stress. Our results indicate a protective role for p23 in PD-related programmed cell death. The data also underscore the involvement of ER, caspases, and the proteasomal system in ER stress-induced cell death process.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.