ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2007
The glial response to CNS HIV infection includes p53 activation and increased expression of p53 target genes.
Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Neuroinflammatory and Neurodegenerative Roles of HIV-1 Tat: A Review of Recent Evidence.Advances in experimental medicine and biology · 2026Review
- 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
- Friends Turn Foe-Astrocytes Contribute to Neuronal Damage in NeuroAIDS.Journal of molecular neuroscience : MN · 2019Review
- Effects of HIV-1 Tat on oligodendrocyte viability are mediated by CaMKIIβ-GSK3β interactions.Journal of neurochemistry · 2019Article
- Induction of a Senescence-Like Phenotype in Cultured Human Fetal Microglia During HIV-1 Infection.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018Article
- Review
- Astrocyte Senescence and Metabolic Changes in Response to HIV Antiretroviral Therapy Drugs.Frontiers in aging neuroscience · 2017Article
- Human immunodeficiency virus protein Tat induces oligodendrocyte injury by enhancing outward KNeurobiology of disease · 2017Article
- Oligodendrocyte Injury and Pathogenesis of HIV-1-Associated Neurocognitive Disorders.Brain sciences · 2016Review
- A Novel Role of Proline Oxidase in HIV-1 Envelope Glycoprotein-induced Neuronal Autophagy.The Journal of biological chemistry · 2015Article
- Oligodendrocytes Are Targets of HIV-1 Tat: NMDA and AMPA Receptor-Mediated Effects on Survival and Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- p53 as a retrovirus-induced oxidative stress modulator.The Journal of general virology · 2015Article
- The p53 Transcriptional Network Influences Microglia Behavior and Neuroinflammation.Critical reviews in immunology · 2015Review
- Redox control of microglial function: molecular mechanisms and functional significance.Antioxidants & redox signaling · 2014Review
- Alteration of select gene expression patterns in individuals infected with HIV-1.Journal of medical virology · 2014Article
- The p53 transcription factor modulates microglia behavior through microRNA-dependent regulation of c-Maf.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Systems analysis of human brain gene expression: mechanisms for HIV-associated neurocognitive impairment and common pathways with Alzheimer's disease.BMC medical genomics · 2013Article
- Article
- Role of p53 in neurodegenerative diseases.Neuro-degenerative diseases · 2012Review
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
HIV-associated dementia (HAD) is a chronic neuroinflammatory disease that remains an important clinical problem without available rational treatment. As HIV does not infect neurons, the pathogenesis of HAD is thought to be secondary to the impact of infected leukocytes, including parenchymal microglia, which can secrete inflammatory mediators and viral products that alter the function of surrounding uninfected cells. We previously reported that the transcription factor p53 accumulates in neurons, microglia, and astrocytes of HAD patients. We have also shown that microglia from p53-deficient mice fail to induce neurotoxicity in response to the HIV coat protein gp120 in a coculture system, supporting the hypothesis that p53 plays a pathogenic role in the chronic neuroinflammatory component of HIV-associated neurodegeneration. We analyzed the extent and cell type specificity of p53 accumulation in subcortical white matter of ten AIDS patients that had previously been shown to demonstrate white matter p53 accumulation. To determine if p53 activation functioned to alter gene expression in HAD, cortical tissue sections were also immunolabeled for the p53 target genes Bax and p21(WAF1). These studies reveal that microglia, astrocytes, and oligodendrocytes all demonstrate p53 activation in response to HIV infection. We observed immunoreactivity for both Bax and p21(WAF1) in neurons and glia from patients demonstrating elevated p53 immunoreactivity. Our findings demonstrate that widespread increased p53 expression is present in HAD. Activation of p53 mediated pathways in the glia of HAD patients may contribute to the neuroinflammatory processes that promote neurodegeneration by inhibiting glial proliferation and/or promoting glial cell dysfunction.
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Registered trials
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.