ArticleASN neuro2012
Protein carbonylation and aggregation precede neuronal apoptosis induced by partial glutathione depletion.
Article in ASN neuro, 2012. 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, 47 citations in OpenAlex.
- Diabetic retinopathy: shaped by the "hidden hand" of post-translational modifications.Molecular neurodegeneration · 2026Review
- Oxidative Stress Promotes Axonal Atrophy through Alterations in Microtubules and EB1 Function.Aging and disease · 2024Article
- Elevated Plasma Protein Carbonyl Concentration Is Associated with More Abnormal White Matter in People with HIV.Viruses · 2023Article
- Diet as a Source of Acrolein: Molecular Basis of Aldehyde Biological Activity in Diabetes and Digestive System Diseases.International journal of molecular sciences · 2023Review
- Small molecule inhibitors of the mitochondrial ClpXP protease possess cytostatic potential and re-sensitize chemo-resistant cancers.Scientific reports · 2021Article
- Sildenafil Alleviates Murine Experimental Autoimmune Encephalomyelitis by Triggering Autophagy in the Spinal Cord.Frontiers in immunology · 2021Article
- Acrolein: A Potential Mediator of Oxidative Damage in Diabetic Retinopathy.Biomolecules · 2020Review
- Microbial ageing and longevity.Nature reviews. Microbiology · 2019Review
- Loss of glutathione redox homeostasis impairs proteostasis by inhibiting autophagy-dependent protein degradation.Cell death and differentiation · 2019Article
- Spermine oxidase: A promising therapeutic target for neurodegeneration in diabetic retinopathy.Pharmacological research · 2019Review
- Mechanism of Protein Carbonylation in Glutathione-Depleted Rat Brain Slices.Neurochemical research · 2018Article
- Biological Implications of Differential Expression of Mitochondrial-Shaping Proteins in Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2017Article
- 58-F, a flavanone from Ophiopogon japonicus, prevents hepatocyte death by decreasing lysosomal membrane permeability.Scientific reports · 2016Article
- Fluorescence labeling of carbonylated lipids and proteins in cells using coumarin-hydrazide.Redox biology · 2015Article
- Neuroprotective effect of paeoniflorin on HExperimental and therapeutic medicine · 2015Article
- β-amyloid fibrils in Alzheimer disease are not inert when bound to copper ions but can degrade hydrogen peroxide and generate reactive oxygen species.The Journal of biological chemistry · 2014Article
- Intermittent hypoxia-induced increases in reactive oxygen species activate NFATc3 increasing endothelin-1 vasoconstrictor reactivity.Vascular pharmacology · 2014Article
- Involvement of reactive oxygen species in a feed-forward mechanism of Na/K-ATPase-mediated signaling transduction.The Journal of biological chemistry · 2013Article
- A comparative study of protein carbonylation and mitochondrial dysfunction using the neurotoxicants 1,3-dinitrobenzene, 3-nitropropionic acid, and 3-chloropropanediol.Neurotoxicology · 2013Article
- Increased carbonylation, protein aggregation and apoptosis in the spinal cord of mice with experimental autoimmune encephalomyelitis.ASN neuro · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
While the build-up of oxidized proteins within cells is believed to be toxic, there is currently no evidence linking protein carbonylation and cell death. In the present study, we show that incubation of nPC12 (neuron-like PC12) cells with 50 μM DEM (diethyl maleate) leads to a partial and transient depletion of glutathione (GSH). Concomitant with GSH disappearance there is increased accumulation of PCOs (protein carbonyls) and cell death (both by necrosis and apoptosis). Immunocytochemical studies also revealed a temporal/spatial relationship between carbonylation and cellular apoptosis. In addition, the extent of all three, PCO accumulation, protein aggregation and cell death, augments if oxidized proteins are not removed by proteasomal degradation. Furthermore, the effectiveness of the carbonyl scavengers hydralazine, histidine hydrazide and methoxylamine at preventing cell death identifies PCOs as the toxic species. Experiments using well-characterized apoptosis inhibitors place protein carbonylation downstream of the mitochondrial transition pore opening and upstream of caspase activation. While the study focused mostly on nPC12 cells, experiments in primary neuronal cultures yielded the same results. The findings are also not restricted to DEM-induced cell death, since a similar relationship between carbonylation and apoptosis was found in staurosporine- and buthionine sulfoximine-treated nPC12 cells. In sum, the above results show for the first time a causal relationship between carbonylation, protein aggregation and apoptosis of neurons undergoing oxidative damage. To the best of our knowledge, this is the first study to place direct (oxidative) protein carbonylation within the apoptotic pathway.
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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.