Evidence map›Paper›PMID 24305723›Full record

ArticleNeuro-oncology2014

Blockade of Kv1.3 channels ameliorates radiation-induced brain injury.

Ying Peng, Kui Lu, Zichen Li, Yaodong Zhao, Yiping Wang, Bin Hu, Pengfei Xu, Xiaolei Shi, Bin Zhou, Michael Pennington and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

49 citing papers in PubMed, 76 citations in OpenAlex.

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  10. Peripheral Administration of the Kv1.3-Blocking Peptide HsTX1[R14A] Improves Cognitive Performance in Senescence Accelerated SAMP8 Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
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  15. Microglia as Therapeutic Target for Radiation-Induced Brain Injury.International journal of molecular sciences · 2022
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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

12 authors at 5 institutions in 2 countries.

Ying PengDepartment of Neurology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China (Y.P., K.L., Z.L., Y.W., B.H., P.X., X.S., Y.T.); Department of Neurosurgery, Shanghai 10th People's Hospital, Tongji University, Shanghai, China (Y.Z., B.Z.); Peptides International, Louisville, Kentucky (M.P.); Department of Physiology and Biophysics, University of California, Irvine, Irvine, California (K.G.C.).
Kui Lu
Zichen Li
Yaodong Zhao
Yiping Wang
Bin Hu
Pengfei Xu
Xiaolei Shi
Bin Zhou
Michael Pennington
K George Chandy
Yamei Tang
Sun Yat-sen University · CNTongji University · CNUniversity of California, Irvine · USPeptides International (United States) · USSun Yat-sen Memorial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumors affecting the head, neck, and brain account for significant morbidity and mortality. The curative efficacy of radiotherapy for these tumors is well established, but radiation carries a significant risk of neurologic injury. So far, neuroprotective therapies for radiation-induced brain injury are still limited. In this study we demonstrate that Stichodactyla helianthus (ShK)-170, a specific inhibitor of the voltage-gated potassium (Kv)1.3 channel, protected mice from radiation-induced brain injury.

methodsMice were treated with ShK-170 for 3 days immediately after brain irradiation. Radiation-induced brain injury was assessed by MRI scans and a Morris water maze. Pathophysiological change of the brain was measured by immunofluorescence. Gene and protein expressions of Kv1.3 and inflammatory factors were measured by quantitative real-time PCR, reverse transcription PCR, ELISA assay, and western blot analyses. Kv currents were recorded in the whole-cell configuration of the patch-clamp technique.

resultsRadiation increased Kv1.3 mRNA and protein expression in microglia. Genetic silencing of Kv1.3 by specific short interference RNAs or pharmacological blockade with ShK-170 suppressed radiation-induced production of the proinflammatory factors interleukin-6, cyclooxygenase-2, and tumor necrosis factor-α by microglia. ShK-170 also inhibited neurotoxicity mediated by radiation-activated microglia and promoted neurogenesis by increasing the proliferation of neural progenitor cells.

conclusionsThe therapeutic effect of ShK-170 is mediated by suppression of microglial activation and microglia-mediated neurotoxicity and enhanced neurorestoration by promoting proliferation of neural progenitor cells.

Indexed as

AnimalsAnimals, NewbornBlotting, WesternBrainBrain InjuriesCnidarian VenomsEnzyme-Linked Immunosorbent AssayImmunoenzyme TechniquesImmunoprecipitationKv1.3 Potassium ChannelMaleMiceMice, Inbred BALB CMicrogliaNeuronsPotassium Channel BlockersCnidarian VenomsKv1.3 Potassium ChannelPotassium Channel BlockersRNA, MessengerRNA, Small InterferingShK neurotoxinKv1.3microgliaradiationShK

Identifiers

PMID24305723
PMCPMC3956348
OpenAlexW2143827181

What OpenQuestion holds

Textmetadata
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.