ArticleThe Journal of biological chemistry2015
Amyloid Oligomers and Mature Fibrils Prepared from an Innocuous Protein Cause Diverging Cellular Death Mechanisms.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Broken but not beaten: Challenge of reducing the amyloids pathogenicity by degradation.Journal of advanced research · 2025Review
- Multimer Detection System: A Universal Assay System for Differentiating Protein Oligomers from Monomers.International journal of molecular sciences · 2025Review
- Choice of Protein, Not Its Amyloid-Fold, Determines the Success of Amyloid-Based Scaffolds for Cartilage Tissue Regeneration.ACS omega · 2023Article
- Modulation of cytotoxic amyloid fibrillation and mitochondrial damage of α-synuclein by catechols mediated conformational changes.Scientific reports · 2023Article
- New Evidence on a Distinction between Aβ40 and Aβ42 Amyloids: Thioflavin T Binding Modes, Clustering Tendency, Degradation Resistance, and Cross-Seeding.International journal of molecular sciences · 2022Article
- Origin, toxicity and characteristics of two amyloid oligomer polymorphs.RSC chemical biology · 2021Article
- Surface-Directed Structural Transition of Amyloidogenic Aggregates and the Resulting Neurotoxicity.ACS omega · 2020Article
- Silk fibroin safety in the eye: a review that highlights a concern.BMJ open ophthalmology · 2020Review
- Amyloid fragments and their toxicity on neural cells.Regenerative biomaterials · 2019Article
- Self-assembling peptide and protein amyloids: from structure to tailored function in nanotechnology.Chemical Society reviews · 2017Review
- Sequestration of Ribosome during Protein Aggregate Formation: Contribution of ribosomal RNA.Scientific reports · 2017Article
- Brain amyloid in preclinical Alzheimer's disease is associated with increased driving risk.Alzheimer's & dementia (Amsterdam, Netherlands) · 2017Article
- Biochemical and Electrophysiological Modification of Amyloid Transthyretin on Cardiomyocytes.Biophysical journal · 2016Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite significant advances, the molecular identity of the cytotoxic species populated during in vivo amyloid formation crucial for the understanding of neurodegenerative disorders is yet to be revealed. In this study lysozyme prefibrillar oligomers and fibrils in both mature and sonicated states have been isolated through an optimized ultrafiltration/ultracentrifugation method and characterized with various optical spectroscopic techniques, atomic force microscopy, and transmission electron microscopy. We examined their level and mode of toxicity on rat pheochromocytoma (PC12) cells in both differentiated and undifferentiated states. We find that oligomers and fibrils display cytotoxic capabilities toward cultured cells in vitro, with oligomers producing elevated levels of cellular injury toward undifferentiated PC12 cells (PC12(undiff)). Furthermore, dual flow cytometry staining experiments demonstrate that the oligomers and mature fibrils induce divergent cellular death pathways (apoptosis and secondary necrosis, respectively) in these PC12 cells. We have also shown that oligomers but not sonicated mature fibrils inhibit hippocampal long term potentiation, a form of synaptic plasticity implicated in learning and memory, in vivo. We conclude that our in vitro and in vivo findings confer a level of resistance toward amyloid fibrils, and that the PC 12-based comparative cytotoxicity assay can provide insights into toxicity differences between differently aggregated protein species.
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