Evidence map›Paper›PMID 16338743›Full record

ArticleJournal of neurovirology2005

Critical implication of the (70-96) domain of human immunodeficiency virus type 1 Vpr protein in apoptosis of primary rat cortical and striatal neurons.

Emmanuelle N Sabbah, Bernard P Roques

Abstract read
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In one paragraph

Article in Journal of neurovirology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-weighted citation impact, top 40% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
  2. Review
  3. Emerging Role of Nef in the Development of HIV Associated Neurological Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021
    Review
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  6. Article
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  12. Review
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  15. Methamphetamine abuse, HIV infection, and neurotoxicity.International journal of physiology, pathophysiology and pharmacology · 2009
    Article
  16. Host and viral factors influencing the pathogenesis of HIV-associated neurocognitive disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2009
    Review
  17. Article
  18. Review
  19. HIV-1 Vpr causes neuronal apoptosis and in vivo neurodegeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Emmanuelle N SabbahUnite de Pharmacochimie Moleculaire et Structurale, INSERM U266, CNRS UMR 8600, UFR des Sciences Pharmaceutiques et Biologiques, Universite Rene Descartes, Paris, France.
Bernard P Roques
Inserm · FRLaboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human immunodeficiency virus (HIV)-1 regulatory protein Vpr has been detected in the serum of HIV-seropositive individuals and in the cerebrospinal fluid of acquired immunodeficiency syndrome (AIDS) patients suffering from neurological disorders. Therefore, Vpr could play a critical role in the neuronal apoptosis observed postmortem in the brain of patients, often connected to a severe AIDS-related disease termed HIV-associated dementia (HAD). This suggests that the Vpr neurotoxicity already observed in vitro on hippocampal neurons could also occur in other brain structures. In this study the authors have investigated the ability of synthetic Vpr to induce apoptosis in primary cultures of rat cortical and striatal neurons. Moreover, the authors have explored the Vpr minimal proapoptotic region using synthetic Vpr fragments and mutants of the protein. Treatments of both neuronal types with Vpr, its C-terminal domain, Vpr(52-96), or a shorter fragment, Vpr(70-96), led to dose- and time-dependent cell death as determined by flow cytometry after propidium iodide labeling, phase-contrast microscopy, and TUNEL labeling. Taken together, these results support an apoptosis-induced death of these neurons. The (71-82) Vpr peptide, previously shown toxic to isolated mitochondria, was inactive on neurons. Vpr-induced neuronal apoptosis was associated with activation of caspase-3 beginning 3 h after Vpr extracellular addition and peaking 3 h later. Moreover, an hyperproduction of reactive oxygen species was observed. In addition to hippocampal neurons, the extension of the apoptotic property of Vpr to cortical and striatal neurons could account for several signs observed in HAD and is thus consistent with a possible involvement of Vpr in this syndrome.

Indexed as

AIDS Dementia ComplexAnimalsApoptosisCerebral CortexCorpus StriatumGene Products, vprHIV-1HIV Envelope Protein gp120HumansNeuronsRatsvpr Gene Products, Human Immunodeficiency VirusGene Products, vprHIV Envelope Protein gp120vpr Gene Products, Human Immunodeficiency Virus

Identifiers

PMID16338743
OpenAlexW2027955847

What OpenQuestion holds

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Registered trials

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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.