Evidence map›Paper›PMID 19891735›Full record

ArticleJournal of neurochemistry2010

Multi-targeted neuroprotection by the HSV-2 gene ICP10PK includes robust bystander activity through PI3-K/Akt and/or MEK/ERK-dependent neuronal release of vascular endothelial growth factor and fractalkine.

Jennifer M Laing, Cynthia C Smith, Laure Aurelian

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Fractalkine and Neuroinflammation in Autism Spectrum Disorder: A Novel Perspective.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025
    Article
  3. Article
  4. [AttenuatedNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  5. Review
  6. Article
  7. GABAPsychopharmacology · 2019
    Review
  8. Article
  9. Review
  10. Review
  11. CRF-amplified neuronal TLR4/MCP-1 signaling regulates alcohol self-administration.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. HSV Recombinant Vectors for Gene Therapy.The open virology journal · 2010
    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.

Jennifer M LaingDepartment of Pharmacology and Experimental Therapeutics, School of Medicine, University of Maryland, Baltimore, Maryland 21201-1559, USA.
Cynthia C Smith
Laure Aurelian
University of Maryland, Baltimore · US

Funding

Neuroprotection and ERK activation by HSV-2 gene ICP10PKR01NS045169 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI AURELIAN, LAURE · 2003 to 2007
$1.7M
NINDS NIH HHS NS45169NINDS NIH HHS R01 NS045169
6 · The paper itself

Abstract

Hippocampal cultures infected with the DeltaRR vector for the HSV-2 anti-apoptotic gene ICP10PK survive cell death triggered by a wide variety of insults. Survival includes robust protection of uninfected neurons, but the mechanism of this bystander activity is still unclear. Here we report that ICP10PK+ neurons release soluble factors that protect uninfected neurons from NMDA and MPP+-induced apoptosis. Release depends on ICP10PK-mediated activation of the Ras signaling pathways MEK/ERK and PI3-K/Akt, and it was not seen for cultures infected with the ICP10PK negative vector DeltaPK. The released neuroprotective factors include vascular endothelial growth factor (VEGF) and fractalkine, the levels of which were significantly higher in conditioned media from hippocampal cultures infected with DeltaRR (NCM(DeltaRR)) than DeltaPK or phosphate-buffered saline (mock infection). VEGF neutralization inhibited the neuroprotective activity of NCM(DeltaRR), indicating that the VEGF protective function is through neuron-neuron cross-talk. NCM(DeltaRR) also stimulated microglia to release increased levels of IL-10 and decreased levels of TNF-alpha that were protective for uninfected neurons. These release patterns were not seen for microglia given NCM(DeltaRR) in which fractalkine was neutralized, indicating that the fractalkine protective function is through bidirectional neuron-microglia communication. Collectively, the data indicate that DeltaRR is a multiple target strategy to rescue neurons from excitotoxic injury.

Indexed as

Analysis of VarianceAnimalsAnimals, NewbornCell CommunicationCells, CulturedCerebral CortexChemokine CX3CL1Chlorocebus aethiopsCulture Media, ConditionedEmbryo, MammalianEnzyme InhibitorsEnzyme-Linked Immunosorbent AssayExtracellular Signal-Regulated MAP KinasesGenetic VectorsHippocampusIn Situ Nick-End LabelingChemokine CX3CL1Culture Media, ConditionedEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesICP10 protein, herpes simplex virus type 2Interleukin-10N-MethylaspartateOncogene Protein v-aktPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-rafRibonucleotide ReductasesTubb3 protein, ratTubulinTumor Necrosis Factor-alphaVascular Endothelial Growth Factor A

Identifiers

PMID19891735
PMCPMC3787133
OpenAlexW2060698197

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.