miR-19a-3p and miR-19b-3p repress Nurr1 and Nur77 to promote microglial inflammation after spinal cord injury

Autores
Sahebdel, Faezeh; Zia, Aliabbas; Quintá, Héctor Ramiro; Stucky, Andres; Morse, Leslie R.; Olson, Julie K.; Battaglino, Ricardo A.
Año de publicación
2026
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Background: Spinal cord injury (SCI)-induced neuropathic pain affects up to 60% of individuals with SCI and is closely linked to microglia-driven neuroinflammation. Neuroinflammatory processes after SCI are major contributors to the development and persistence of chronic pain. MicroRNAs (miRNAs) have emerged as regulators of neuroinflammation. There are higher levels of circulating miR-19a and miR-19b in persons living with SCI with neuropathic pain compared to those with no pain. These miRNAs are associated with altered the neuroprotective genes Nurr1 and Nur77.Methods: Primary microglia cultures and a rat spinal cord injury model were used to investigate the regulatory effects of miR-19a and miR-19b on Nurr1 and Nur77 expression.Results: Our study shows that miR-19a and miR-19b and their binding sites in Nurr1’s 3′ UTR are highly conserved across vertebrates, suggesting functional importance. Through in vitro microglia cultures and in vivo rat SCI models, we demonstrate that these miRNAs negatively regulate Nurr1, Nur77, and inflammatory gene expression. Protein–protein interaction network analysis highlights transcription factors such as MYC, RUNX1, and STAT3 as central to this regulatory network.Conclusion: These findings support a model in which miR-19a and miR-19b contribute to microglia-driven neuroinflammation after SCI and highlight their potential as therapeutic targets to reduce neuropathic pain.
Fil: Sahebdel, Faezeh. Miami University; Estados Unidos
Fil: Zia, Aliabbas. University of Montreal; Canadá
Fil: Quintá, Héctor Ramiro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán; Argentina
Fil: Stucky, Andres. Miami University; Estados Unidos
Fil: Morse, Leslie R.. Miami University; Estados Unidos
Fil: Olson, Julie K.. University of Minnesota; Estados Unidos
Fil: Battaglino, Ricardo A.. Miami University; Estados Unidos
Materia
LESIÓN DE MÉDULA ESPINAL
NETRIN
NURR
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/286528
Acceder
id CONICETDig_ded83906950cec5417bfd88fae536e66
oai_identifier_str oai:ri.conicet.gov.ar:11336/286528
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling miR-19a-3p and miR-19b-3p repress Nurr1 and Nur77 to promote microglial inflammation after spinal cord injurySahebdel, FaezehZia, AliabbasQuintá, Héctor RamiroStucky, AndresMorse, Leslie R.Olson, Julie K.Battaglino, Ricardo A.LESIÓN DE MÉDULA ESPINALNETRINNURRhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Background: Spinal cord injury (SCI)-induced neuropathic pain affects up to 60% of individuals with SCI and is closely linked to microglia-driven neuroinflammation. Neuroinflammatory processes after SCI are major contributors to the development and persistence of chronic pain. MicroRNAs (miRNAs) have emerged as regulators of neuroinflammation. There are higher levels of circulating miR-19a and miR-19b in persons living with SCI with neuropathic pain compared to those with no pain. These miRNAs are associated with altered the neuroprotective genes Nurr1 and Nur77.Methods: Primary microglia cultures and a rat spinal cord injury model were used to investigate the regulatory effects of miR-19a and miR-19b on Nurr1 and Nur77 expression.Results: Our study shows that miR-19a and miR-19b and their binding sites in Nurr1’s 3′ UTR are highly conserved across vertebrates, suggesting functional importance. Through in vitro microglia cultures and in vivo rat SCI models, we demonstrate that these miRNAs negatively regulate Nurr1, Nur77, and inflammatory gene expression. Protein–protein interaction network analysis highlights transcription factors such as MYC, RUNX1, and STAT3 as central to this regulatory network.Conclusion: These findings support a model in which miR-19a and miR-19b contribute to microglia-driven neuroinflammation after SCI and highlight their potential as therapeutic targets to reduce neuropathic pain.Fil: Sahebdel, Faezeh. Miami University; Estados UnidosFil: Zia, Aliabbas. University of Montreal; CanadáFil: Quintá, Héctor Ramiro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán; ArgentinaFil: Stucky, Andres. Miami University; Estados UnidosFil: Morse, Leslie R.. Miami University; Estados UnidosFil: Olson, Julie K.. University of Minnesota; Estados UnidosFil: Battaglino, Ricardo A.. Miami University; Estados UnidosFrontiers Media2026-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/286528Sahebdel, Faezeh; Zia, Aliabbas; Quintá, Héctor Ramiro; Stucky, Andres; Morse, Leslie R.; et al.; miR-19a-3p and miR-19b-3p repress Nurr1 and Nur77 to promote microglial inflammation after spinal cord injury; Frontiers Media; Frontiers in Cellular Neuroscience; 20; 3-2026; 1-131662-5102CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fncel.2026.1783899/fullinfo:eu-repo/semantics/altIdentifier/doi/10.3389/fncel.2026.1783899info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2026-08-25T14:36:10Zoai:ri.conicet.gov.ar:11336/286528instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982026-08-25 14:36:10.711CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv miR-19a-3p and miR-19b-3p repress Nurr1 and Nur77 to promote microglial inflammation after spinal cord injury
title miR-19a-3p and miR-19b-3p repress Nurr1 and Nur77 to promote microglial inflammation after spinal cord injury
spellingShingle miR-19a-3p and miR-19b-3p repress Nurr1 and Nur77 to promote microglial inflammation after spinal cord injury
Sahebdel, Faezeh
LESIÓN DE MÉDULA ESPINAL
NETRIN
NURR
title_short miR-19a-3p and miR-19b-3p repress Nurr1 and Nur77 to promote microglial inflammation after spinal cord injury
title_full miR-19a-3p and miR-19b-3p repress Nurr1 and Nur77 to promote microglial inflammation after spinal cord injury
title_fullStr miR-19a-3p and miR-19b-3p repress Nurr1 and Nur77 to promote microglial inflammation after spinal cord injury
title_full_unstemmed miR-19a-3p and miR-19b-3p repress Nurr1 and Nur77 to promote microglial inflammation after spinal cord injury
title_sort miR-19a-3p and miR-19b-3p repress Nurr1 and Nur77 to promote microglial inflammation after spinal cord injury
dc.creator.none.fl_str_mv Sahebdel, Faezeh
Zia, Aliabbas
Quintá, Héctor Ramiro
Stucky, Andres
Morse, Leslie R.
Olson, Julie K.
Battaglino, Ricardo A.
author Sahebdel, Faezeh
author_facet Sahebdel, Faezeh
Zia, Aliabbas
Quintá, Héctor Ramiro
Stucky, Andres
Morse, Leslie R.
Olson, Julie K.
Battaglino, Ricardo A.
author_role author
author2 Zia, Aliabbas
Quintá, Héctor Ramiro
Stucky, Andres
Morse, Leslie R.
Olson, Julie K.
Battaglino, Ricardo A.
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv LESIÓN DE MÉDULA ESPINAL
NETRIN
NURR
topic LESIÓN DE MÉDULA ESPINAL
NETRIN
NURR
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Background: Spinal cord injury (SCI)-induced neuropathic pain affects up to 60% of individuals with SCI and is closely linked to microglia-driven neuroinflammation. Neuroinflammatory processes after SCI are major contributors to the development and persistence of chronic pain. MicroRNAs (miRNAs) have emerged as regulators of neuroinflammation. There are higher levels of circulating miR-19a and miR-19b in persons living with SCI with neuropathic pain compared to those with no pain. These miRNAs are associated with altered the neuroprotective genes Nurr1 and Nur77.Methods: Primary microglia cultures and a rat spinal cord injury model were used to investigate the regulatory effects of miR-19a and miR-19b on Nurr1 and Nur77 expression.Results: Our study shows that miR-19a and miR-19b and their binding sites in Nurr1’s 3′ UTR are highly conserved across vertebrates, suggesting functional importance. Through in vitro microglia cultures and in vivo rat SCI models, we demonstrate that these miRNAs negatively regulate Nurr1, Nur77, and inflammatory gene expression. Protein–protein interaction network analysis highlights transcription factors such as MYC, RUNX1, and STAT3 as central to this regulatory network.Conclusion: These findings support a model in which miR-19a and miR-19b contribute to microglia-driven neuroinflammation after SCI and highlight their potential as therapeutic targets to reduce neuropathic pain.
Fil: Sahebdel, Faezeh. Miami University; Estados Unidos
Fil: Zia, Aliabbas. University of Montreal; Canadá
Fil: Quintá, Héctor Ramiro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán; Argentina
Fil: Stucky, Andres. Miami University; Estados Unidos
Fil: Morse, Leslie R.. Miami University; Estados Unidos
Fil: Olson, Julie K.. University of Minnesota; Estados Unidos
Fil: Battaglino, Ricardo A.. Miami University; Estados Unidos
description Background: Spinal cord injury (SCI)-induced neuropathic pain affects up to 60% of individuals with SCI and is closely linked to microglia-driven neuroinflammation. Neuroinflammatory processes after SCI are major contributors to the development and persistence of chronic pain. MicroRNAs (miRNAs) have emerged as regulators of neuroinflammation. There are higher levels of circulating miR-19a and miR-19b in persons living with SCI with neuropathic pain compared to those with no pain. These miRNAs are associated with altered the neuroprotective genes Nurr1 and Nur77.Methods: Primary microglia cultures and a rat spinal cord injury model were used to investigate the regulatory effects of miR-19a and miR-19b on Nurr1 and Nur77 expression.Results: Our study shows that miR-19a and miR-19b and their binding sites in Nurr1’s 3′ UTR are highly conserved across vertebrates, suggesting functional importance. Through in vitro microglia cultures and in vivo rat SCI models, we demonstrate that these miRNAs negatively regulate Nurr1, Nur77, and inflammatory gene expression. Protein–protein interaction network analysis highlights transcription factors such as MYC, RUNX1, and STAT3 as central to this regulatory network.Conclusion: These findings support a model in which miR-19a and miR-19b contribute to microglia-driven neuroinflammation after SCI and highlight their potential as therapeutic targets to reduce neuropathic pain.
publishDate 2026
dc.date.none.fl_str_mv 2026-03
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/286528
Sahebdel, Faezeh; Zia, Aliabbas; Quintá, Héctor Ramiro; Stucky, Andres; Morse, Leslie R.; et al.; miR-19a-3p and miR-19b-3p repress Nurr1 and Nur77 to promote microglial inflammation after spinal cord injury; Frontiers Media; Frontiers in Cellular Neuroscience; 20; 3-2026; 1-13
1662-5102
CONICET Digital
CONICET
url http://hdl.handle.net/11336/286528
identifier_str_mv Sahebdel, Faezeh; Zia, Aliabbas; Quintá, Héctor Ramiro; Stucky, Andres; Morse, Leslie R.; et al.; miR-19a-3p and miR-19b-3p repress Nurr1 and Nur77 to promote microglial inflammation after spinal cord injury; Frontiers Media; Frontiers in Cellular Neuroscience; 20; 3-2026; 1-13
1662-5102
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fncel.2026.1783899/full
info:eu-repo/semantics/altIdentifier/doi/10.3389/fncel.2026.1783899
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Frontiers Media
publisher.none.fl_str_mv Frontiers Media
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.24418

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