ArticleNeuroscience2015
Forebrain neuronal specific ablation of p53 gene provides protection in a cortical ischemic stroke model.
Article in Neuroscience, 2015. 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, 31 citations in OpenAlex.
- Partial FAM19A5 deficiency in mice leads to disrupted spine maturation, hyperactivity, and an altered fear response.PloS one · 2025Article
- Intracellular FGF1 protects cells from apoptosis through direct interaction with p53.Cellular and molecular life sciences : CMLS · 2023Article
- Regulation of the p53‑mediated ferroptosis signaling pathway in cerebral ischemia stroke (Review).Experimental and therapeutic medicine · 2023Review
- Monocyte, neutrophil, and whole blood transcriptome dynamics following ischemic stroke.BMC medicine · 2023Article
- MDMX elevation by a novel Mdmx-p53 interaction inhibitor mitigates neuronal damage after ischemic stroke.Scientific reports · 2022Article
- Diphtheria toxin induced but not CSF1R inhibitor mediated microglia ablation model leads to the loss of CSF/ventricular spaces in vivo that is independent of cytokine upregulation.Journal of neuroinflammation · 2022Article
- Genetic Deficiency of p53 Leads to Structural, Functional, and Synaptic Deficits in Primary Somatosensory Cortical Neurons of Adult Mice.Frontiers in molecular neuroscience · 2022Article
- Differential Role of p53 in Oligodendrocyte Survival in Response to Various Stresses: Experimental Autoimmune Encephalomyelitis, Cuprizone Intoxication or White Matter Stroke.International journal of molecular sciences · 2021Article
- 17β-Estradiol Abrogates Oxidative Stress and Neuroinflammation after Cortical Stab Wound Injury.Antioxidants (Basel, Switzerland) · 2021Article
- Review
- Hesperidin Ameliorates Anxiety-Depressive-Like Behavior in 6-OHDA Model of Parkinson's Disease by Regulating Striatal Cytokine and Neurotrophic Factors Levels and Dopaminergic Innervation Loss in the Striatum of Mice.Molecular neurobiology · 2020Article
- The unique expression profile of FAM19A1 in the mouse brain and its association with hyperactivity, long-term memory and fear acquisition.Scientific reports · 2020Article
- The p53 inactivators pifithrin-μ and pifithrin-α mitigate TBI-induced neuronal damage through regulation of oxidative stress, neuroinflammation, autophagy and mitophagy.Experimental neurology · 2020Article
- Dopaminergic Neuron-Specific Deletion of p53 Gene Attenuates Methamphetamine Neurotoxicity.Neurotoxicity research · 2017Article
- Neurotrophic and neuroprotective effects of oxyntomodulin in neuronal cells and a rat model of stroke.Experimental neurology · 2017Article
- Novel pharmaceutical treatments for minimal traumatic brain injury and evaluation of animal models and methodologies supporting their development.Journal of neuroscience methods · 2016Review
- Dopaminergic neuron-specific deletion of p53 gene is neuroprotective in an experimental Parkinson's disease model.Journal of neurochemistry · 2016Article
- Effect of the sonic hedgehog receptor smoothened on the survival and function of dopaminergic neurons.Experimental neurology · 2016Article
- Stanniocalcin-1 Protects a Mouse Model from Renal Ischemia-Reperfusion Injury by Affecting ROS-Mediated Multiple Signaling Pathways.International journal of molecular sciences · 2016Article
- Notch signaling and neuronal death in stroke.Progress in neurobiologyReview
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Cerebral ischemic injury involves death of multiple cell types at the ischemic sites. As a key regulator of cell death, the p53 gene has been implicated in the regulation of cell loss in stroke. Less focal damage is found in stroke animals pre-treated with a p53 inhibitor or in traditional p53 knockout (ko) mice. However, whether the p53 gene plays a direct role in regulating neuronal cell death is unknown. In this study, in contrast to the global inhibition of p53 function by pharmacological inhibitors and in traditional p53 ko mice, we utilized a neuronal specific conditional ko mouse line (CamcreTRP53(loxP/loxP)) to achieve forebrain neuronal specific deletion of p53 and examined the role of the p53 gene in ischemia-induced cell death in neurons. Expression of p53 after stroke is examined using the immunohistochemical method and the outcome of stroke is examined by analysis of infarction size and behavioral deficits caused by stroke. Our data showed that p53 expression is upregulated in the ischemic region in neuronal cells in wildtype (wt) mice but not in CamcreTRP53(loxP/loxP) ko mice. Deletion of the p53 gene in forebrain neurons results in a decreased infarction area in ko mice. Locomotor behavior, measured in automated activity chambers, showed that CamcreTRP53(loxP/loxP) ko mice have less locomotor deficits compared to wt mice after middle cerebral artery occlusion (MCAo). We conclude that manipulation of p53 expression in neurons may lead to unique therapeutic development in stroke.
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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.