Evidence map›Paper›PMID 22016798›Full record

ArticlePloS one2011

HIV-1gp120 induces neuronal apoptosis through enhancement of 4-aminopyridine-senstive outward K+ currents.

Lina Chen, Jianuo Liu, Changshui Xu, James Keblesh, Weijin Zang, Huangui Xiong

Abstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

34 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  17. Oxidative Stress during HIV Infection: Mechanisms and Consequences.Oxidative medicine and cellular longevity · 2016
    Review
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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

6 authors.

Lina ChenNeurophysiology Laboratory, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
Jianuo Liu
Changshui Xu
James Keblesh
Weijin Zang
Huangui Xiong

Funding

Therapeutics Core (Page 286)P30MH062261 · NIMH · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI GENDELMAN, HOWARD E · 2000 to 2021
$37.7M
Pharmacokinetics and Drug-Drug InteractionsP01DA028555 · NIDA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI ALNOUTI, YAZEN · 2010 to 2019
$16.8M
NEURONAL PHYSIOLOGY AND HIV-1 ASSOCIATED DEMENTIAR01NS041862 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI XIONG, HUANGUI HANK · 2001 to 2009
$2.3M
NIDA NIH HHS P01 DA028555NIMH NIH HHS P30 MH062261NINDS NIH HHS 2R01NS041862NINDS NIH HHS R01 NS041862
6 · The paper itself

Abstract

Human immunodeficiency virus type 1 (HIV-1)-associated dementia (HAD) usually occurs late in the course of HIV-1 infection and the mechanisms underlying HAD pathogenesis are not well understood. Accumulating evidence indicates that neuronal voltage-gated potassium (Kv) channels play an important role in memory processes and acquired neuronal channelopathies in HAD. To examine whether Kv channels are involved in HIV-1-associated neuronal injury, we studied the effects of HIV-1 glycoprotein 120 (gp120) on outward K+ currents in rat cortical neuronal cultures using whole-cell patch techniques. Exposure of cortical neurons to gp120 produced a dose-dependent enhancement of A-type transient outward K+ currents (IA). The gp120-induced increase of IA was attenuated by T140, a specific antagonist for chemokine receptor CXCR4, suggesting gp120 enhancement of neuronal IA via CXCR4. Pretreatment of neuronal cultures with a protein kinase C (PKC) inhibitor, GF109203X, inhibited the gp120-induced increase of IA. Biological significance of gp120 enhancement of IA was demonstrated by experimental results showing that gp120-induced neuronal apoptosis, as detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and caspase-3 staining, was attenuated by either an IA blocker 4-aminopyridine or a specific CXCR4 antagonist T140. Taken together, these results suggest that gp120 may induce caspase-3 dependent neuronal apoptosis by enhancing IA via CXCR4-PKC signaling.

Indexed as

4-AminopyridineAnimalsApoptosisCaspase 3Cells, CulturedCerebral CortexDrug SynergismEnzyme ActivationFemaleHIV Envelope Protein gp120NeuronsOligopeptidesPotassiumPotassium Channel BlockersPregnancyProtein Kinase C4-AminopyridineCaspase 3Cxcr4 protein, ratgp120 protein, Human immunodeficiency virus 1HIV Envelope Protein gp120OligopeptidesPotassiumPotassium Channel BlockersProtein Kinase CReceptors, CXCR4T140 peptide

Identifiers

PMID22016798
PMCPMC3189248

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.