Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/3662
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dc.contributor.authorVay, Sabine Ulrikeen_US
dc.contributor.authorFlitsch, Lea Jessicaen_US
dc.contributor.authorRabenstein, Monikaen_US
dc.contributor.authorMonière, Helenaen_US
dc.contributor.authorJakovcevski, Igoren_US
dc.contributor.authorAndjus, Pavleen_US
dc.contributor.authorBijelic, Dunjaen_US
dc.contributor.authorBlaschke, Stefanen_US
dc.contributor.authorWalter, Helene Luiseen_US
dc.contributor.authorFink, Gereon Rudolfen_US
dc.contributor.authorSchroeter, Michaelen_US
dc.contributor.authorRueger, Maria Adeleen_US
dc.date.accessioned2020-11-26T15:45:17Z-
dc.date.available2020-11-26T15:45:17Z-
dc.date.issued2020-04-06-
dc.identifier.citationVay SU, Flitsch LJ, Rabenstein M, Monière H, Jakovcevski I, Andjus P, Bijelic D, Blaschke S, Walter HL, Fink GR, Schroeter M, Rueger MA. The impact of hyperpolarization-activated cyclic nucleotide-gated (HCN) and voltage-gated potassium KCNQ/Kv7 channels on primary microglia function. J Neuroinflammation. 2020 Apr 6;17(1):100. doi: 10.1186/s12974-020-01779-4. PMID: 32248813; PMCID: PMC7132998.en_US
dc.identifier.issn1742-2094-
dc.identifier.urihttps://biore.bio.bg.ac.rs/handle/123456789/3662-
dc.description.abstractBackground: Microglia 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 results: Under 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. Conclusion: These 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.en_US
dc.relation.ispartofJournal of Neuroinflammationen_US
dc.subjectCerebral ischemiaen_US
dc.subjectIh-currenten_US
dc.subjectIon channelen_US
dc.subjectMicroglia activationen_US
dc.subjectMicroglia phenotypeen_US
dc.subjectMigrationen_US
dc.subjectNeuroinflammationen_US
dc.subjectPhagocytosisen_US
dc.subjectVoltage sensor probesen_US
dc.subjectXE-991en_US
dc.subjectZD7288en_US
dc.subjectsiHCN2en_US
dc.titleThe impact of hyperpolarization-activated cyclic nucleotide-gated (HCN) and voltage-gated potassium KCNQ/Kv7 channels on primary microglia functionen_US
dc.typeArticleen_US
dc.identifier.doi10.1186/s12974-020-01779-4-
dc.identifier.pmid32248813-
dc.description.rankM21a-
dc.description.impact8.322-
item.cerifentitytypePublications-
item.openairetypeArticle-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.deptChair of General Physiology and Biophysics-
crisitem.author.deptChair of General Physiology and Biophysics-
crisitem.author.orcid0000-0002-8468-8513-
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