ArticleAge (Dordrecht, Netherlands)2015
Cytochrome b5 reductase, a plasma membrane redox enzyme, protects neuronal cells against metabolic and oxidative stress through maintaining redox state and bioenergetics.
Article in Age (Dordrecht, Netherlands), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
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- Intracellular imaging of metmyoglobin and oxygen using new dual purpose probe EYFP-Myoglobin-mCherry.Journal of biophotonics · 2022Article
- Type-A response regulators negatively mediate heat stress response by altering redox homeostasis in Arabidopsis.Frontiers in plant science · 2022Article
- A New Insight into an Alternative Therapeutic Approach to Restore Redox Homeostasis and Functional Mitochondria in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- The Pro-Oxidant Activity of Red Wine Polyphenols Induces an Adaptive Antioxidant Response in Human Erythrocytes.Antioxidants (Basel, Switzerland) · 2021Article
- Increasing Nrf2 Activity as a Treatment Approach in Neuropsychiatry.Molecular neurobiology · 2021Review
- Review
- Oxidative stress, autophagy and airway ion transport.American journal of physiology. Cell physiology · 2019Review
- Cellular and Molecular Mechanisms of Recessive Hereditary Methaemoglobinaemia Type II.Journal of clinical medicine · 2018Review
- Collaborating genomic, transcriptomic and microbiomic alterations lead to canine extreme intestinal polyposis.Oncotarget · 2018Article
- How Supraphysiological Oxygen Levels in Standard Cell Culture Affect Oxygen-Consuming Reactions.Oxidative medicine and cellular longevity · 2018Review
- Influence of anaerobic and aerobic exercise on age-related pathways in skeletal muscle.Ageing research reviews · 2017Review
- Cytochrome b5 protects photoreceptors from light stress-induced lipid peroxidation and retinal degeneration.NPJ aging and mechanisms of disease · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The plasma membrane redox system (PMRS) containing NADH-dependent reductases is known to be involved in the maintenance of redox state and bioenergetics. Neuronal cells are very vulnerable to oxidative stress and altered energy metabolism linked to mitochondrial dysfunction. However, the role of the PMRS in these pathways is far from clear. In this study, in order to investigate how cytochrome b5 reductase (b5R), one of the PM redox enzymes, regulates cellular response under stressed conditions, human neuroblastoma cells transfected with b5R were used for viability and mitochondrial functional assays. Cells transfected with b5R exhibited significantly higher levels of the NAD(+)/NADH ratio, consistent with increased levels of b5R activity. Overexpression of b5R made cells more resistant to H2O2 (oxidative stress), 2-deoxyglucose (metabolic stress), rotenone and antimycin A (energetic stress), and lactacystin (proteotoxic stress), but did not protect cells against H2O2 and serum withdrawal. Overexpression of b5R induced higher mitochondrial functions such as ATP production rate, oxygen consumption rate, and activities of complexes I and II, without formation of further reactive oxygen species, consistent with lower levels of oxidative/nitrative damage and resistance to apoptotic cell death. In conclusion, higher NAD(+)/NADH ratio and consequent more efficient mitochondrial functions are induced by the PMRS, enabling them to maintain redox state and energy metabolism under conditions of some energetic stresses. This suggests that b5R can be a target for therapeutic intervention for aging and neurodegenerative diseases.
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