Evidence map›Paper›PMID 19306367›Full record

ArticleGlia2009

Enhancement of neuronal outward delayed rectifier K+ current by human monocyte-derived macrophages.

Dehui Hu, Jianuo Liu, Huangui Xiong

Abstract read
In one paragraph

Article in Glia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Enhancement of NMDA receptor-mediated excitatory postsynaptic currents by gp120-treated macrophages: implications for HIV-1-associated neuropathology.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013
    Article
  7. Review
  8. Article
  9. HIV-associated neurocognitive disorder: pathogenesis and therapeutic opportunities.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010
    Review
  10. Article
  11. 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

3 authors at 1 institution in 1 country.

Dehui HuNeurophysiology Laboratory, Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska 68198-5880, USA.
Jianuo Liu
Huangui Xiong
University of Nebraska Medical Center · US

Funding

NEURONAL PHYSIOLOGY AND HIV-1 ASSOCIATED DEMENTIAR01NS041862 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI XIONG, HUANGUI HANK · 2001 to 2009
$2.3M
NINDS NIH HHS 2 R01 NS041862NINDS NIH HHS R01 NS041862
6 · The paper itself

Abstract

Macrophages are critical cells in mediating the pathology of neurodegenerative disorders and enhancement of neuronal outward potassium (K(+)) current has implicated in neuronal apoptosis. To understand how activated macrophages induce neuronal dysfunction and injury, we studied the effects of lipopolysaccharide (LPS)-stimulated human monocytes-derived macrophage (MDM) on neuronal outward delayed rectifier K(+) current (I(K)) and resultant change on neuronal viability in primary rat hippocampal neuronal culture. Bath application of LPS-stimulated MDM-conditioned media (MCM) enhanced neuronal I(K) in a concentration-dependent manner, whereas non-stimulated MCM failed to alter neuronal I(K). The enhancement of neuronal I(K) was repeated in a macrophage-neuronal co-culture system. The link of stimulated MCM (MCM(+))-associated enhancement of I(K) to MCM(+)-induced neuronal injury, as detected by PI/DAPI (propidium iodide/4',6-diamidino-2-phenylindol) staining and MTT assay, was demonstrated by experimental results showing that addition of I(K) blocker tetraethylammonium to the culture protected hippocampal neurons from MCM(+)-associated challenge. Further investigation revealed elevated levels of K(v) 1.3 and K(v) 1.5 channel expression in hippocampal neurons after addition of MCM(+) to the culture. These results suggest that during brain inflammation macrophages, through their capacity of releasing bioactive molecules, induce neuronal injury by enhancing neuronal I(K) and that modulation of K(v) channels is a new approach to neuroprotection.

Indexed as

AnimalsCells, CulturedCell SurvivalCoculture TechniquesDelayed Rectifier Potassium ChannelsHippocampusHumansKv1.3 Potassium ChannelKv1.5 Potassium ChannelLipopolysaccharidesMacrophagesMembrane PotentialsMonocytesNeuronsPotassiumPotassium Channel BlockersDelayed Rectifier Potassium ChannelsKv1.3 Potassium ChannelKv1.5 Potassium ChannelLipopolysaccharidesPotassiumPotassium Channel BlockersTetraethylammonium

Identifiers

PMID19306367
PMCPMC2744853
OpenAlexW2114709051

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.