Evidence map›Paper›PMID 32248813›Full record

ArticleJournal of neuroinflammation2020

The impact of hyperpolarization-activated cyclic nucleotide-gated (HCN) and voltage-gated potassium KCNQ/Kv7 channels on primary microglia function.

Sabine Ulrike Vay, Lea Jessica Flitsch, Monika Rabenstein, Helena Monière, Igor Jakovcevski, Pavle Andjus, Dunja Bijelic, Stefan Blaschke, Helene Luise Walter, Gereon Rudolf Fink and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Designing Neural Dynamics: From Digital Twin Modeling to Regeneration.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Glial KCNQ KNeuron · 2024
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Acute Treatment with the M-Channel (KNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Deleterious Alteration of Glia in the Brain of Alzheimer's Disease.International journal of molecular sciences · 2020
    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

12 authors at 4 institutions in 2 countries.

Sabine Ulrike VayDepartment of Neurology, Faculty of Medicine and University Hospital, University Hospital of Cologne, Kerpener Strasse 62, 50924, Cologne, Germany. sabine.vay@uk-koeln.de.
Lea Jessica FlitschDepartment of Neurology, Faculty of Medicine and University Hospital, University Hospital of Cologne, Kerpener Strasse 62, 50924, Cologne, Germany.
Monika RabensteinDepartment of Neurology, Faculty of Medicine and University Hospital, University Hospital of Cologne, Kerpener Strasse 62, 50924, Cologne, Germany.
Helena MonièreDepartment of Neurology, Faculty of Medicine and University Hospital, University Hospital of Cologne, Kerpener Strasse 62, 50924, Cologne, Germany.
Igor JakovcevskiInstitute for Molecular and Behavioural Neuroscience and Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany.
Pavle AndjusCenter for Laser Microscopy-CLM, Faculty of Biology, University of Belgrade, Belgrade, Serbia.
Dunja BijelicCenter for Laser Microscopy-CLM, Faculty of Biology, University of Belgrade, Belgrade, Serbia.
Stefan BlaschkeDepartment of Neurology, Faculty of Medicine and University Hospital, University Hospital of Cologne, Kerpener Strasse 62, 50924, Cologne, Germany.
Helene Luise WalterDepartment of Neurology, Faculty of Medicine and University Hospital, University Hospital of Cologne, Kerpener Strasse 62, 50924, Cologne, Germany.
Gereon Rudolf FinkDepartment of Neurology, Faculty of Medicine and University Hospital, University Hospital of Cologne, Kerpener Strasse 62, 50924, Cologne, Germany.
Michael SchroeterDepartment of Neurology, Faculty of Medicine and University Hospital, University Hospital of Cologne, Kerpener Strasse 62, 50924, Cologne, Germany.
Maria Adele RuegerDepartment of Neurology, Faculty of Medicine and University Hospital, University Hospital of Cologne, Kerpener Strasse 62, 50924, Cologne, Germany.
University Hospital Cologne · DEUniversity of Belgrade · RSForschungszentrum Jülich · DEUniversity of Cologne · DE

Funding

Deutscher Akademischer Austauschdienst 57393537Marga und Walter Boll-Stiftung 210-10-15Science and Technology Development Center, Ministry of Education III41005Universität zu Köln 345/2018
6 · The paper itself

Abstract

backgroundMicroglia are essential to maintain cell homeostasis in the healthy brain and are activated after brain injury. Upon activation, microglia polarize towards different phenotypes. The course of microglia activation is complex and depends on signals in the surrounding milieu. Recently, it has been suggested that microglia respond to ion currents, as a way of regulating their activity and function. METHODS AND

resultsUnder the hypothesis that HCN and KCNQ/Kv7 channels impact on microglia, we studied primary rat microglia in the presence or absence of specific pharmacological blockade or RNA silencing. Primary microglia expressed the subunits HCN1-4, Kv7.2, Kv7.3, and Kv7.5. The expression of HCN2, as well as Kv7.2 and Kv7.3, varied among different microglia phenotypes. The pharmacological blockade of HCN channels by ZD7288 resulted in cell depolarization with slowly rising intracellular calcium levels, leading to enhanced survival and reduced proliferation rates of resting microglia. Furthermore, ZD7288 treatment, as well as knockdown of HCN2 RNA by small interfering RNA, resulted in an attenuation of later microglia activation-both towards the anti- and pro-inflammatory phenotype. However, HCN channel inhibition enhanced the phagocytic capacity of IL4-stimulated microglia. Blockade of Kv7/KCNQ channel by XE-991 exclusively inhibited the migratory capacity of resting microglia.

conclusionThese observations suggest that the HCN current contributes to various microglia functions and impacts on the course of microglia activation, while the Kv7/KCNQ channels affect microglia migration. Characterizing the role of HCN channels in microglial functioning may offer new therapeutic approaches for targeted modulation of neuroinflammation as a hallmark of various neurological disorders.

Indexed as

AnimalsCalciumCell ProliferationHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsMicrogliaPhagocytosisPotassium Channel BlockersPotassium Channels, Voltage-GatedPyrimidinesRatsRats, WistarRNA InterferenceCalciumHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsICI D2788Potassium Channel BlockersPotassium Channels, Voltage-GatedPyrimidinesCerebral ischemiaIh-currentIon channelMicroglia activationMicroglia phenotypeMigrationNeuroinflammationPhagocytosissiHCN2Voltage sensor probesXE-991ZD7288

Identifiers

PMID32248813
PMCPMC7132998
OpenAlexW3015173695

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.