ArticleScientific reports2016
Differences in vulnerability of neurons and astrocytes to heme oxygenase-1 modulation: Implications for mitochondrial ferritin.
Article in Scientific reports, 2016. 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, 32 citations in OpenAlex.
- Notoginsenoside R1 Attenuates Oxidative Damage After Intracerebral Hemorrhage by Inhibiting LCN2 and Promoting HO-1 in Astrocytes.Brain sciences · 2026Article
- Review
- CHEX-seq detects single-cell genomic single-stranded DNA with catalytical potential.Nature communications · 2023Article
- The effects of Korean Red Ginseng on heme oxygenase-1 with a focus on mitochondrial function in pathophysiologic conditions.Journal of ginseng research · 2023Review
- Vitamin K2 (MK-7) attenuates LPS-induced acute lung injury via inhibiting inflammation, apoptosis, and ferroptosis.PloS one · 2023Article
- Beneficial and Detrimental Roles of Heme Oxygenase-1 in the Neurovascular System.International journal of molecular sciences · 2022Review
- Review
- Importance of Heme Oxygenase-1 in Gastrointestinal Cancers: Functions, Inductions, Regulations, and Signaling.Journal of gastrointestinal cancer · 2021Review
- Article
- Ammonia-Induced Glial-Inflammaging.Molecular neurobiology · 2020Article
- The Chemical Basis of Intracerebral Hemorrhage and Cell Toxicity With Contributions From Eryptosis and Ferroptosis.Frontiers in cellular neuroscience · 2020Article
- Hepcidin-to-Ferritin Ratio Is Decreased in Astrocytes With Extracellular Alpha-Synuclein and Iron Exposure.Frontiers in cellular neuroscience · 2020Article
- The Role of Astrocytes in the Central Nervous System Focused on BK Channel and Heme Oxygenase Metabolites: A Review.Antioxidants (Basel, Switzerland) · 2019Review
- Iron in Neurodegeneration - Cause or Consequence?Frontiers in neuroscience · 2019Review
- Mitochondrial superoxide generation induces a parkinsonian phenotype in zebrafish and huntingtin aggregation in human cells.Free radical biology & medicine · 2019Article
- A review on heme oxygenase-1 induction: is it a necessary evil.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Review
- Neurotoxicity Linked to Dysfunctional Metal Ion Homeostasis and Xenobiotic Metal Exposure: Redox Signaling and Oxidative Stress.Antioxidants & redox signaling · 2018Review
- Astroglial DJ-1 over-expression up-regulates proteins involved in redox regulation and is neuroprotective in vivo.Redox biology · 2018Article
- HACE1 is essential for astrocyte mitochondrial function and influences Huntington disease phenotypes in vivo.Human molecular genetics · 2018Article
- "Pumping iron"-how macrophages handle iron at the systemic, microenvironmental, and cellular levels.Pflugers Archiv : European journal of physiology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Induction of the antioxidant enzyme heme oxygenase-1 (HO-1) was observed in both astrocytes and neurons in the substantia nigra of patients with Parkinson's disease (PD). In the current study, we investigated whether HO-1 behaves differently between neurons and astrocytes under the condition of neurotoxicity related to PD. The results showed a time-dependent HO-1 upregulation in primary cultured ventral mesencephalon neurons and astrocytes treated with the mitochondria complex I inhibitor 1-methyl-4-phenylpyridinium (MPP(+)) or recombinant α-synuclein. However, HO-1 upregulation appeared much later in neurons than in astrocytes. The HO-1 inhibitor zinc protoporphyrin (ZnPP) aggravated MPP(+)- or α-synuclein-induced oxidative damage in both astrocytes and neurons, indicating that this HO-1 response was cytoprotective. For neurons, the HO-1 activator cobalt protoporphyrin IX (CoPPIX) exerted protective effects against MPP(+) or α-synuclein during moderate HO-1 upregulation, but it aggravated damage at the peak of the HO-1 response. For astrocytes, CoPPIXalways showed protective effects. Higher basal and CoPPIX-induced mitochondrial ferritin (MtFt) levels were detected in astrocytes. Lentivirus-mediated MtFt overexpression rescued the neuronal damage induced by CoPPIX, indicating that large MtFt buffering capacity contributes to pronounced HO-1 tolerance in astrocytes. Such findings suggest that astrocyte-targeted HO-1 interventions and MtFt modulations have potential as novel pharmacological strategies in PD.
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