Evidence map›Paper›PMID 25623966›Full record

ArticleNeuropharmacology2015

Pharmacological induction of CCL5 in vivo prevents gp120-mediated neuronal injury.

Lee A Campbell, Valeriya Avdoshina, Chris Day, Seung T Lim, Italo Mocchetti

Abstract read
In one paragraph

Article in Neuropharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Lee A CampbellDepartment of Pharmacology and Physiology, Laboratory of Preclinical Neurobiology, Georgetown University Medical Center, Washington, D.C. 20057, USA; Department of Neuroscience, Laboratory of Preclinical Neurobiology, Georgetown University Medical Center, Washington, D.C. 20057, USA.
Valeriya AvdoshinaDepartment of Neuroscience, Laboratory of Preclinical Neurobiology, Georgetown University Medical Center, Washington, D.C. 20057, USA.
Chris DayDepartment of Neuroscience, Laboratory of Preclinical Neurobiology, Georgetown University Medical Center, Washington, D.C. 20057, USA.
Seung T LimDepartment of Neuroscience, Laboratory of Preclinical Neurobiology, Georgetown University Medical Center, Washington, D.C. 20057, USA.
Italo MocchettiDepartment of Neuroscience, Laboratory of Preclinical Neurobiology, Georgetown University Medical Center, Washington, D.C. 20057, USA. Electronic address: moccheti@georgetown.edu.
Georgetown University Medical Center · USGeorgetown University · US

Funding

Role of proBNDF and p75NTR in HIV-mediated Axonal/Dendritic DegenerationR01NS079172 · NINDS · GEORGETOWN UNIVERSITY · PI Italo Mocchetti · 2012 to 2026
$7.0M
HIV drug abusers, polymorphisms and brain plasticityR01DA026174 · NIDA · GEORGETOWN UNIVERSITY · PI MOCCHETTI, ITALO · 2008 to 2012
$1.8M
Mechanisms of morphine mediated neuroprotection against gp120Bal toxicity.F31DA032282 · NIDA · GEORGETOWN UNIVERSITY · PI CAMPBELL, LEE · 2011 to 2013
$126k
NIDA NIH HHS DA026174NIDA NIH HHS F31 DA032282NIDA NIH HHS F31DA032282NIDA NIH HHS R01 DA026174NINDS NIH HHS NS079172NINDS NIH HHS R01 NS079172
6 · The paper itself

Abstract

The human immunodeficiency virus (HIV) envelope protein gp120 promotes neuronal injury which is believed to cause HIV-associated neurocognitive disorders. Therefore, blocking the neurotoxic effect of gp120 may lead to alternative strategies to reduce the neurotoxic effect of HIV. In vitro, the neurotoxic effect of M-tropic gp120BaL is reduced by the chemokine CCL5, the natural ligand of CCR5 receptors. To determine whether CCL5 reduces the toxic effect of gp120BaL in vivo, animals were intrastriatally injected with lentiviral vectors overexpressing CCL5 prior to an intrastriatal injection of gp120BaL (400 ng). Neuronal injury was determined by silver staining, cleaved caspase-3 and TUNEL. Overexpression of CCL5 decreased gp120-mediated neuronal injury. CCL5 expression can be up-regulated by chronic morphine. Therefore, we examined whether morphine reduces the neurotoxic effect of gp120BaL. Rats stereotaxically injected with gp120BaL into the striatum received saline or chronic morphine for five days (10 mg/kg escalating to 30 mg/kg twice a day). Morphine-treated rats showed a decrease in all markers used to determine neuronal degeneration compared to saline-treated rats. The neuroprotective effect of morphine was significantly attenuated by expressing CCL5 shRNA. Our results suggest that compounds that increase the endogenous production of CCL5 may be used to reduce the pathogenesis of HIV-associated neurocognitive disorders.

Indexed as

Brain InjuriesAnimalsAstrocytesCadherinsCaspase 3Cells, CulturedCerebral CortexChemokine CCL5Embryo, MammalianHIV Envelope Protein gp120HumansMaleMorphineNeuronsProtocadherinsRatsCadherinsCaspase 3Chemokine CCL5gp120 protein, Human immunodeficiency virus 1HIV Envelope Protein gp120MorphinePcdh1 protein, mouseProtocadherinsRNA, Small InterferingCaspase-3CCL5-lentivirusIL-1βMorphine withdrawalNeurodegenerationNeuroprotection

Identifiers

PMID25623966
PMCPMC4346538
OpenAlexW1993197724

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.