Pharmacological Inhibition of Microglial Proliferation Supports Blood–Brain Barrier Integrity in Experimental Autoimmune Encephalomyelitis

Blood–brain barrier dysfunction (BBB) is a primary characteristic of experimental autoimmune encephalomyelitis (EAE), an experimental model of multiple sclerosis (MS). We have previously shown that blocking microglial proliferation using GW2580, a selective inhibitor of CSF1R (Colony stimulating fac...

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Autores: Borjini, Nozha, Fernandez, Mercedes, Giardino, Luciana, Sorokin, Lydia, Calzà, Laura
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2025
País:España
Institución:Universidad de Sevilla (US)
Repositorio:idUS. Depósito de Investigación de la Universidad de Sevilla
OAI Identifier:oai:idus.us.es:11441/174461
Acceso en línea:https://hdl.handle.net/11441/174461
https://doi.org/10.3390/cells14060414
Access Level:acceso abierto
Palabra clave:Microglia
Blood–brain barrier
Experimental autoimmune encephalomyelitis
Multiple sclerosis
GW2580
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spelling Pharmacological Inhibition of Microglial Proliferation Supports Blood–Brain Barrier Integrity in Experimental Autoimmune EncephalomyelitisBorjini, NozhaFernandez, MercedesGiardino, LucianaSorokin, LydiaCalzà, LauraMicrogliaBlood–brain barrierExperimental autoimmune encephalomyelitisMultiple sclerosisGW2580Blood–brain barrier dysfunction (BBB) is a primary characteristic of experimental autoimmune encephalomyelitis (EAE), an experimental model of multiple sclerosis (MS). We have previously shown that blocking microglial proliferation using GW2580, a selective inhibitor of CSF1R (Colony stimulating factor 1 receptor), reduced disease progression and severity and prevented the relapse phase. However, whether this was due to effects of GW2580 on the functional integrity of the BBB was not determined. Therefore, here, we examine BBB properties in rats during EAE under GW2580 treatment. Our data suggest that blocking early microglial proliferation through selective targeting of CSF1R signaling has a therapeutic effect in EAE by protecting BBB integrity and reducing peripheral immune cell infiltration. Taken together, our results identify a novel mechanism underlying the effects of GW2580, which could offer a novel therapy for MS.MDPIFisiología Médica y BiofísicaEuropean Union (UE)2025info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfapplication/pdfhttps://hdl.handle.net/11441/174461https://doi.org/10.3390/cells14060414reponame:idUS. Depósito de Investigación de la Universidad de Sevillainstname:Universidad de Sevilla (US)InglésCells, 14 (6).FP7-PEOPLE-2013-ITNhttps://www.mdpi.com/2073-4409/14/6/414info:eu-repo/semantics/openAccessoai:idus.us.es:11441/1744612026-06-17T12:51:07Z
dc.title.none.fl_str_mv Pharmacological Inhibition of Microglial Proliferation Supports Blood–Brain Barrier Integrity in Experimental Autoimmune Encephalomyelitis
title Pharmacological Inhibition of Microglial Proliferation Supports Blood–Brain Barrier Integrity in Experimental Autoimmune Encephalomyelitis
spellingShingle Pharmacological Inhibition of Microglial Proliferation Supports Blood–Brain Barrier Integrity in Experimental Autoimmune Encephalomyelitis
Borjini, Nozha
Microglia
Blood–brain barrier
Experimental autoimmune encephalomyelitis
Multiple sclerosis
GW2580
title_short Pharmacological Inhibition of Microglial Proliferation Supports Blood–Brain Barrier Integrity in Experimental Autoimmune Encephalomyelitis
title_full Pharmacological Inhibition of Microglial Proliferation Supports Blood–Brain Barrier Integrity in Experimental Autoimmune Encephalomyelitis
title_fullStr Pharmacological Inhibition of Microglial Proliferation Supports Blood–Brain Barrier Integrity in Experimental Autoimmune Encephalomyelitis
title_full_unstemmed Pharmacological Inhibition of Microglial Proliferation Supports Blood–Brain Barrier Integrity in Experimental Autoimmune Encephalomyelitis
title_sort Pharmacological Inhibition of Microglial Proliferation Supports Blood–Brain Barrier Integrity in Experimental Autoimmune Encephalomyelitis
dc.creator.none.fl_str_mv Borjini, Nozha
Fernandez, Mercedes
Giardino, Luciana
Sorokin, Lydia
Calzà, Laura
author Borjini, Nozha
author_facet Borjini, Nozha
Fernandez, Mercedes
Giardino, Luciana
Sorokin, Lydia
Calzà, Laura
author_role author
author2 Fernandez, Mercedes
Giardino, Luciana
Sorokin, Lydia
Calzà, Laura
author2_role author
author
author
author
dc.contributor.none.fl_str_mv Fisiología Médica y Biofísica
European Union (UE)
dc.subject.none.fl_str_mv Microglia
Blood–brain barrier
Experimental autoimmune encephalomyelitis
Multiple sclerosis
GW2580
topic Microglia
Blood–brain barrier
Experimental autoimmune encephalomyelitis
Multiple sclerosis
GW2580
description Blood–brain barrier dysfunction (BBB) is a primary characteristic of experimental autoimmune encephalomyelitis (EAE), an experimental model of multiple sclerosis (MS). We have previously shown that blocking microglial proliferation using GW2580, a selective inhibitor of CSF1R (Colony stimulating factor 1 receptor), reduced disease progression and severity and prevented the relapse phase. However, whether this was due to effects of GW2580 on the functional integrity of the BBB was not determined. Therefore, here, we examine BBB properties in rats during EAE under GW2580 treatment. Our data suggest that blocking early microglial proliferation through selective targeting of CSF1R signaling has a therapeutic effect in EAE by protecting BBB integrity and reducing peripheral immune cell infiltration. Taken together, our results identify a novel mechanism underlying the effects of GW2580, which could offer a novel therapy for MS.
publishDate 2025
dc.date.none.fl_str_mv 2025
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/11441/174461
https://doi.org/10.3390/cells14060414
url https://hdl.handle.net/11441/174461
https://doi.org/10.3390/cells14060414
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Cells, 14 (6).
FP7-PEOPLE-2013-ITN
https://www.mdpi.com/2073-4409/14/6/414
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv MDPI
publisher.none.fl_str_mv MDPI
dc.source.none.fl_str_mv reponame:idUS. Depósito de Investigación de la Universidad de Sevilla
instname:Universidad de Sevilla (US)
instname_str Universidad de Sevilla (US)
reponame_str idUS. Depósito de Investigación de la Universidad de Sevilla
collection idUS. Depósito de Investigación de la Universidad de Sevilla
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15.198674

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