ArticleCellular and molecular neurobiology2015
Ceruloplasmin is Involved in the Nigral Iron Accumulation of 6-OHDA-Lesioned Rats.
Article in Cellular and molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Pooled it
- Parkinson Disease Signaling Pathways, Molecular Mechanisms, and Potential Therapeutic Strategies: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Glial cells improve Parkinson's disease by modulating neuronal function and regulating neuronal ferroptosis.Frontiers in cell and developmental biology · 2024Review
- Advancements in understanding substantia nigra hyperechogenicity via transcranial sonography in Parkinson's disease and its clinical implications.Frontiers in neurology · 2024Review
- Signaling pathways in Parkinson's disease: molecular mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- DL-3-n-butylphthalide alleviates motor disturbance by suppressing ferroptosis in a rat model of Parkinson's disease.Neural regeneration research · 2023Article
- Aberrant Cerebral Iron Trafficking Co-morbid With Chronic Inflammation: Molecular Mechanisms and Pharmacologic Intervention.Frontiers in neurology · 2022Review
- Neuroprotective effects of kukoamine A on 6-OHDA-induced Parkinson's model through apoptosis and iron accumulation inhibition.Chinese herbal medicines · 2021Article
- Mapping Chemical Elements and Iron Oxidation States in the Substantia Nigra of 6-Hydroxydopamine Lesioned Rats Using Correlative Immunohistochemistry With Proton and Synchrotron Micro-Analysis.Frontiers in neuroscience · 2019Article
- Involvement of Ventral Periaqueductal Gray Dopaminergic Neurons in Propofol Anesthesia.Neurochemical research · 2018Article
- Coherent and Contradictory Facts, Feats and Fictions Associated with Metal Accumulation in Parkinson's Disease: Epicenter or Outcome, Yet a Demigod Question.Molecular neurobiology · 2017Review
- Brain Iron Metabolism Dysfunction in Parkinson's Disease.Molecular neurobiology · 2017Review
- New Insights into the Crosstalk between NMDARs and Iron: Implications for Understanding Pathology of Neurological Diseases.Frontiers in molecular neuroscience · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated iron levels in the substantia nigra (SN) participate in neuronal death in Parkinson's disease (PD), while the mechanisms underlying the increased iron are still unknown. Ceruloplasmin (CP), a ferroxidase, converts highly toxic ferrous iron to its non-toxic ferric form, which cooperated with ferroportin1 (FP1) facilitating the export of iron from cells. To elucidate if the abnormal expression of CP is involved in the nigral iron accumulation, here, we investigated CP expression in the SN of rats lesioned by 6-hydroxydopamine (6-OHDA). We showed that FP1 and CP colocalized in the rat SN. One day after 6-OHDA lesion, when there was a half reduction in the number of dopaminergic neurons, the iron level was increased compared with the normal rats; both the mRNA and protein expressions of CP decreased compared with the control. When rats began showing rotation behavior induced by apomorphine, usually after 6 weeks since 6-OHDA lesion, they are considered PD models. In these PD models, almost no dopaminergic neurons can be detected in the lesioned SN and nigral iron level was further increased. At this time point, a further decrease of CP was observed. These results show that FP1 and CP colocalize in the rat brain, indicating the coordinated actions of the two proteins in the cellular iron export, and suggest that decreased expression of CP in the SN is involved in the nigral iron accumulation of 6-OHDA-lesioned rats.
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