ArticleMolecular neurobiology2014
Alpha-synuclein oligomerization in manganese-induced nerve cell injury in brain slices: a role of NO-mediated S-nitrosylation of protein disulfide isomerase.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Protein disulfide isomerase dissolves and detoxifies oligomeric assemblies of amyloid beta peptide.FEBS letters · 2026Article
- Revisiting cirrhosis-related parkinsonism: a comprehensive review.Metabolic brain disease · 2026Review
- Molecular mechanisms of exercise-induced neuroprotection against Parkinson's disease.Sports medicine and health science · 2026Review
- Common and Trace Metals in Alzheimer's and Parkinson's Diseases.International journal of molecular sciences · 2023Review
- Consequences of Disturbing Manganese Homeostasis.International journal of molecular sciences · 2023Review
- The Role of Protein S-Nitrosylation in Protein Misfolding-Associated Diseases.Life (Basel, Switzerland) · 2021Review
- Review
- POSCAbilities: The Application of the Prion Organotypic Slice Culture Assay to Neurodegenerative Disease Research.Biomolecules · 2020Review
- The Role of Autophagy in Manganese-Induced Neurotoxicity.Frontiers in neuroscience · 2020Review
- Reversal of Alpha-Synuclein Fibrillization by Protein Disulfide Isomerase.Frontiers in cell and developmental biology · 2020Article
- New Insights on the Role of Manganese in Alzheimer's Disease and Parkinson's Disease.International journal of environmental research and public health · 2019Review
- The role of posttranslational modifications of α-synuclein and LRRK2 in Parkinson's disease: Potential contributions of environmental factors.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Mn-Induced Neurocytes Injury and Autophagy Dysfunction in Alpha-Synuclein Wild-Type and Knock-Out Mice: Highlighting the Role of Alpha-Synuclein.Neurotoxicity research · 2019Article
- The Emerging Role of Electrophiles as a Key Regulator for Endoplasmic Reticulum (ER) Stress.International journal of molecular sciences · 2019Review
- PDI-mediated S-nitrosylation of DRP1 facilitates DRP1-S616 phosphorylation and mitochondrial fission in CA1 neurons.Cell death & disease · 2018Article
- The effect of manganese exposure in Atp13a2-deficient mice.Neurotoxicology · 2018Article
- Untangling the Manganese-α-Synuclein Web.Frontiers in neuroscience · 2016Review
- Aberrant protein S-nitrosylation contributes to the pathophysiology of neurodegenerative diseases.Neurobiology of disease · 2015Review
- S-nitrosylation of the thioredoxin-like domains of protein disulfide isomerase and its role in neurodegenerative conditions.Frontiers in chemistry · 2015Review
- ATP13A2 and Alpha-synuclein: a Metal Taste in Autophagy.Experimental neurobiology · 2014Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over-exposure to manganese (Mn) has been known to induce endoplasmic reticulum (ER) stress involving protein misfolding. The proper maturation and folding of native proteins rely on the activity of protein disulfide isomerase (PDI). However, the exact mechanism of Mn-induced alpha-synuclein oligomerization is unclear. To explore whether alpha-synuclein oligomerization was associated with S-nitrosylation of PDI, we made the rat brain slice model of manganism and pretreated slices with L-Canavanine, a selective iNOS inhibitor. After slices were treated with Mn (0, 25, 100, and 400 μM) for 24 h, there were dose-dependent increases in apoptotic percentage of cells, lactate dehydrogenase (LDH) releases, production of NO, inducible nitric oxide synthase (iNOS) activity, the mRNA and protein expressions of iNOS, and PDI. Moreover, S-nitrosylated PDI and alpha-synuclein oligomerization also increased. However, there was a significant increase in the PDI activity of 25-μM Mn-treated slices. Then, PDI activity and the affinity between PDI and alpha-synuclein decreased significantly in response to Mn (100 and 400 μM), which was associated with S-nitrosylation of PDI. The results indicated that S-nitrosylated PDI could affect its activity. We use the L-Canavanine pretreatment brain slices to inhibit S-nitrosylation of PDI. The results showed that L-Canavanine pretreatment could reduce Mn-induced nerve cell injury and alpha-synuclein oligomerization. Additionally, there was a significant recovery in PDI activity in L-Canavanine-pretreated slices. The findings revealed that Mn induced nitrosative stress via the activation of iNOS and subsequent S-nitrosylation of PDI in cultured slices. Moreover, S-nitrosylation of PDI is an important signaling event in the Mn-induced alpha-synuclein oligomerization in brain slices.
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