ArticleStroke2009
Potential role of PUMA in delayed death of hippocampal CA1 neurons after transient global cerebral ischemia.
Article in Stroke, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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Who cites it
56 citing papers in PubMed, 84 citations in OpenAlex.
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Molecular Targeting of Ischemic Stroke: The Promise of Naïve and Engineered Extracellular Vesicles.Pharmaceutics · 2024Review
- Article
- Involvement of Proteasomal and Endoplasmic Reticulum Stress in Neurodegeneration After Global Brain Ischemia.Molecular neurobiology · 2023Article
- Reverse Electron Transport at Mitochondrial Complex I in Ischemic Stroke, Aging, and Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- MDMX elevation by a novel Mdmx-p53 interaction inhibitor mitigates neuronal damage after ischemic stroke.Scientific reports · 2022Article
- Regulation and Role of Neuron-Derived Hemoglobin in the Mouse Hippocampus.International journal of molecular sciences · 2022Article
- Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer's Disease Proteinopathy.Antioxidants (Basel, Switzerland) · 2022Review
- Neuroprotective Mechanism of Icariin on Hypoxic Ischemic Brain Damage in Neonatal Mice.Oxidative medicine and cellular longevity · 2022Article
- Proteasome and Neuroprotective Effect of Hyperbaric Oxygen Preconditioning in Experimental Global Cerebral Ischemia in Rats.Frontiers in neurology · 2022Article
- Insulin resistance in ischemic stroke: Mechanisms and therapeutic approaches.Frontiers in endocrinology · 2022Review
- Article
- How cytosolic compartments play safeguard functions against neuroinflammation and cell death in cerebral ischemia.Metabolic brain disease · 2021Review
- Mesenchymal Stem Cell-Mediated Mitochondrial Transfer: a Therapeutic Approach for Ischemic Stroke.Translational stroke research · 2021Review
- Expression and inhibitory effects of p53-upregulated modulator of apoptosis in gallbladder carcinoma.Oncology letters · 2021Article
- Neuroprotective effects of minocycline on focal cerebral ischemia injury: a systematic review.Neural regeneration research · 2020Review
- Cell Death and Recovery in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- Mode of action of granulocyte-colony stimulating factor (G-CSF) as a novel therapy for stroke in a mouse model.Journal of biomedical science · 2020Article
- Down-regulation of cyclin-dependent kinase 5 attenuates p53-dependent apoptosis of hippocampal CA1 pyramidal neurons following transient cerebral ischemia.Scientific reports · 2019Article
- PretreatedNeural regeneration research · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
background and purposep53-upregulated modulator of apoptosis (PUMA), a BH3-only member of the Bcl-2 protein family, is required for p53-dependent and -independent forms of apoptosis. PUMA localizes to mitochondria and interacts with antiapoptotic Bcl-2 and Bcl-X(L) or proapoptotic Bax in response to death stimuli. Although studies have shown that PUMA is associated with pathomechanisms of cerebral ischemia, clearly defined roles for PUMA in ischemic neuronal death remain unclear. The purpose of this study was to determine potential roles for PUMA in cerebral ischemia.
methodsFive minutes of transient global cerebral ischemia (tGCI) were induced by bilateral common carotid artery occlusion combined with hypotension.
resultsPUMA was upregulated in vulnerable hippocampal CA1 neurons after tGCI as shown by immunohistochemistry. In Western blot and coimmunoprecipitation analyses, PUMA localized to mitochondria and was bound to Bcl-X(L) and Bax in the hippocampal CA1 subregion after tGCI. PUMA upregulation was inhibited by pifithrin-alpha, a specific inhibitor of p53, suggesting that PUMA is partly controlled by the p53 transcriptional pathway after tGCI. Furthermore, reduction in oxidative stress by overexpression of copper/zinc superoxide dismutase, which is known to be protective of vulnerable ischemic hippocampal neurons, inhibited PUMA upregulation and subsequent hippocampal CA1 neuronal death after tGCI.
conclusionsThese results imply a potential role for PUMA in delayed CA1 neuronal death after tGCI and that it could be a molecular target for therapy.
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Registered trials
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