Evidence map›Paper›PMID 22258405›Full record

ArticleCell death & disease2012

Involvement of Kv1.3 and p38 MAPK signaling in HIV-1 glycoprotein 120-induced microglia neurotoxicity.

J Liu, C Xu, L Chen, P Xu, H Xiong

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 2 pooled it
1.2field-weighted citation impact, top 24% 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

37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 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 2 countries.

J LiuNeurophysiology Laboratory, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198-5880, USA.
C Xu
L Chen
P Xu
H Xiong
University of Nebraska Medical Center · USNanchang University · CN

Funding

Therapeutics Core (Page 286)P30MH062261 · NIMH · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI GENDELMAN, HOWARD E · 2000 to 2021
$37.7M
NEURONAL PHYSIOLOGY AND HIV-1 ASSOCIATED DEMENTIAR01NS041862 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI XIONG, HUANGUI HANK · 2001 to 2009
$2.3M
Microglial ion channels and HIV-1-associated dementiaR01NS077873 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI XIONG, HUANGUI HANK · 2012 to 2016
$1.8M
Macrophages, NR2B-containing NMDA Receptors and HIV DementiaR01NS063878 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI XIONG, HUANGUI HANK · 2009 to 2013
$1.8M
Voltage-gated K channels, microglia and HIV DementiaR56NS041862 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI XIONG, HUANGUI HANK · 2010 to 2010
$371k
NIMH NIH HHS P30 MH062261NINDS NIH HHS 2R56 NS041862NINDS NIH HHS 5 R01 NS063878NINDS NIH HHS R01 NS041862NINDS NIH HHS R01 NS041862-9NINDS NIH HHS R01 NS063878NINDS NIH HHS R01 NS077873NINDS NIH HHS R56 NS041862
6 · The paper itself

Abstract

Inflammatory responses mediated by activated microglia play a pivotal role in the pathogenesis of human immunodeficiency virus type 1 (HIV-1)-associated neurocognitive disorders. Studies on identification of specific targets to control microglia activation and resultant neurotoxic activity are imperative. Increasing evidence indicate that voltage-gated K(+) (K(v)) channels are involved in the regulation of microglia functionality. In this study, we investigated K(v)1.3 channels in the regulation of neurotoxic activity mediated by HIV-1 glycoprotein 120 (gp120)-stimulated rat microglia. Our results showed treatment of microglia with gp120 increased the expression levels of K(v)1.3 mRNA and protein. In parallel, whole-cell patch-clamp studies revealed that gp120 enhanced microglia K(v)1.3 current, which was blocked by margatoxin, a K(v)1.3 blocker. The association of gp120 enhancement of K(v)1.3 current with microglia neurotoxicity was demonstrated by experimental results that blocking microglia K(v)1.3 attenuated gp120-associated microglia production of neurotoxins and neurotoxicity. Knockdown of K(v)1.3 gene by transfection of microglia with K(v)1.3-siRNA abrogated gp120-associated microglia neurotoxic activity. Further investigation unraveled an involvement of p38 MAPK in gp120 enhancement of microglia K(v)1.3 expression and resultant neurotoxic activity. These results suggest not only a role K(v)1.3 may have in gp120-associated microglia neurotoxic activity, but also a potential target for the development of therapeutic strategies.

Indexed as

ApoptosisAnimalsAnimals, NewbornCells, CulturedGene Expression RegulationGene SilencingHIV Envelope Protein gp120HumansKv1.3 Potassium ChannelMicrogliaNeuronsNeurotoxinsp38 Mitogen-Activated Protein KinasesPatch-Clamp TechniquesPotassium Channel BlockersRatsHIV Envelope Protein gp120Kv1.3 Potassium ChannelmargatoxinNeurotoxinsp38 Mitogen-Activated Protein KinasesPotassium Channel BlockersRNA, MessengerRNA, Small InterferingScorpion Venoms

Identifiers

PMID22258405
PMCPMC3270274
OpenAlexW2046185940

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.