ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2018
Neuronal expression of the mitochondrial protein prohibitin confers profound neuroprotection in a mouse model of focal cerebral ischemia.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Comparative Brain Proteomic Analysis between Sham and Cerebral Ischemia Experimental Groups.International journal of molecular sciences · 2024Article
- Pan-cancer Analysis Combined with Experiments Deciphers PHB Regulation for Breast Cancer Cell Survival and Predicts Biomarker Function.Combinatorial chemistry & high throughput screening · 2024Article
- Neuron-targeted Knockout of APE1 Forces Premature Cognitive Impairment and Synaptic Dysfunction in Adult Mice.Aging and disease · 2022Article
- Role of Nitric Oxide and Protein S-Nitrosylation in Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2021Review
- Role of Prohibitins in Aging and Therapeutic Potential Against Age-Related Diseases.Frontiers in genetics · 2021Review
- Prohibitin S-Nitrosylation Is Required for the Neuroprotective Effect of Nitric Oxide in Neuronal Cultures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Curcumin: Novel Treatment in Neonatal Hypoxic-Ischemic Brain Injury.Frontiers in physiology · 2019Article
- Prohibitin is a positive modulator of mitochondrial function in PC12 cells under oxidative stress.Journal of neurochemistry · 2018Article
- Significance of prohibitin domain family in tumorigenesis and its implication in cancer diagnosis and treatment.Cell death & disease · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The mitochondrial protein prohibitin (PHB) has emerged as an important modulator of neuronal survival in different injury modalities . We previously showed that viral gene transfer of PHB protects CA1 neurons from delayed neurodegeneration following transient forebrain ischemia through mitochondrial mechanisms. However, since PHB is present in all cell types, it is not known if its selective expression in neurons is protective, and if the protection occurs also in acute focal ischemic brain injury, the most common stroke type in humans. Therefore, we generated transgenic mice overexpressing human PHB1 specifically in neurons (PHB1 Tg). PHB1 Tg mice and littermate controls were subjected to transient middle cerebral artery occlusion (MCAo). Infarct volume and sensory-motor impairment were assessed three days later. Under the control of a neuronal promoter (CaMKIIα), PHB1 expression was increased by 50% in the forebrain and hippocampus in PHB1 Tg mice. The brain injury produced by MCAo was reduced by 63 ± 11% in PHB1 Tg mice compared to littermate controls. This reduction was associated with improved sensory-motor performance, suggesting that the salvaged brain remains functional. Approaches to enhance PHB expression may be useful to ameliorate the devastating impact of cerebral ischemia on the brain.
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Registered trials
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