Evidence map›Paper›PMID 23551718›Full record

ArticleThe European journal of neuroscience2013

Transcriptome profiling of hippocampal CA1 after early-life seizure-induced preconditioning may elucidate new genetic therapies for epilepsy.

L K Friedman, J Mancuso, A Patel, V Kudur, J R Leheste, S Iacobas, J Botta, D A Iacobas, D C Spray

Abstract read
In one paragraph

Article in The European journal of neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

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  8. [Regulatory mechanism of MS275 on the p38 MAPK signaling pathway in rats with convulsion in the developmental stage].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2020
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  20. Kv5, Kv6, Kv8, and Kv9 subunits: No simple silent bystanders.The Journal of general physiology · 2016
    Review
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

9 authors at 5 institutions in 1 country.

L K FriedmanBasic Sciences, Cell Biology & Anatomy, New York Medical College, 50 Dana Rd, Valhalla, NY 10595, USA. Linda_Friedman@nymc.edu
J Mancuso
A Patel
V Kudur
J R Leheste
S Iacobas
J Botta
D A Iacobas
D C Spray
Albert Einstein College of Medicine · USPhiladelphia College of Osteopathic Medicine · USAlabama College of Osteopathic Medicine · USNew York Institute of Technology · USYork University · US

Funding

The Astrocyte Nexus: CX43-Protein InteractionsR01NS041282 · NINDS · YESHIVA UNIVERSITY · PI SPRAY, DAVID C · 2002 to 2011
$3.3M
"Connexin-Dependent Transcriptomic Networks in Controlling the Heart Rhythm"R01HL092001 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI IACOBAS, DUMITRU ANDREI · 2009 to 2010
$830k
NHLBI NIH HHS R01 HL092001NINDS NIH HHS NIH NS041282NINDS NIH HHS R01 NS041282
6 · The paper itself

Abstract

Injury of the CA1 subregion induced by a single injection of kainic acid (1 × KA) in juvenile animals (P20) is attenuated in animals with two prior sustained neonatal seizures on P6 and P9. To identify gene candidates involved in the spatially protective effects produced by early-life conditioning seizures we profiled and compared the transcriptomes of CA1 subregions from control, 1 × KA- and 3 × KA-treated animals. More genes were regulated following 3 × KA (9.6%) than after 1 × KA (7.1%). Following 1 × KA, genes supporting oxidative stress, growth, development, inflammation and neurotransmission were upregulated (e.g. Cacng1, Nadsyn1, Kcng1, Aven, S100a4, GFAP, Vim, Hrsp12 and Grik1). After 3 × KA, protective genes were differentially over-expressed [e.g. Cat, Gpx7, Gad1, Hspa12A, Foxn1, adenosine A1 receptor, Ca(2+) adaptor and homeostasis proteins, Cacnb4, Atp2b2, anti-apoptotic Bcl-2 gene members, intracellular trafficking protein, Grasp and suppressor of cytokine signaling (Socs3)]. Distinct anti-inflammatory interleukins (ILs) not observed in adult tissues [e.g. IL-6 transducer, IL-23 and IL-33 or their receptors (IL-F2 )] were also over-expressed. Several transcripts were validated by real-time polymerase chain reaction (QPCR) and immunohistochemistry. QPCR showed that casp 6 was increased after 1 × KA but reduced after 3 × KA; the pro-inflammatory gene Cox1 was either upregulated or unchanged after 1 × KA but reduced by ~70% after 3 × KA. Enhanced GFAP immunostaining following 1 × KA was selectively attenuated in the CA1 subregion after 3 × KA. The observed differential transcriptional responses may contribute to early-life seizure-induced pre-conditioning and neuroprotection by reducing glutamate receptor-mediated Ca(2+) permeability of the hippocampus and redirecting inflammatory and apoptotic pathways. These changes could lead to new genetic therapies for epilepsy.

Indexed as

TranscriptomeAge FactorsAnimalsCA1 Region, HippocampalGene Expression ProfilingGenetic TherapyKainic AcidRatsRats, Sprague-DawleySeizuresTranscription, GeneticKainic Acidcalciumconditioningdevelopmenthippocampusmicroarrayseizures

Identifiers

PMID23551718
PMCPMC4354696
OpenAlexW2090883038

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.