The endocannabinoid anandamide mediates anti‐inflammatory effects through activation of NR4A nuclear receptors

Autores
Teichmann, Tom; Pflüger Mülle, Beatrice; Martín Giménez, Virna Margarita; Sailer, Fiona; Dirks, Henrik; Zehr, Simonida; Warwick, Timothy; Brettner, Felix; Munoz Tello, Paola; Zimmer, Andreas; Tegeder, Irmgard; Thomas, Dominique; Gurke, Robert; Günther, Stefan; Heering, Jan; Proschak, Ewgenij; Geisslinger, Gerd; Bibli, Iris S.; Meyer zu Heringdorf, Dagmar; Manucha, Walter Ariel Fernando; Windbergs, Maike; Knapp, Stefan; Weigert, Andreas; Leisegang, Matthias S.; Kojetin, Douglas; Brandes, Ralf P.
Año de publicación
2024
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Endocannabinoids are lipid mediators, which elicit complex biological effects that extend beyond the central nervous system. The tissue concentrations of endocannabinoids increase in atherosclerosis, and for the endocannabinoid N-arachidonoyl-ethanolamine (anandamide; AEA), this has been linked to a potential anti-inflammatory function. Focusing on vascular smooth muscle cells, we set out to determine the underlying mechanism. Confirming previous results, AEA pretreatment attenuated the cytokine-mediated induction of inflammatory gene expression like CCL2. Unexpectedly, this effect was also observed in preparations of cannabinoid receptor (CB) 1 and 2 knockout mice and after pertussis toxin treatment but was restricted to fairly high concentrations of the lipid. The anti-inflammatory effect of AEA required preincubation, suggesting an effect through gene induction. RNA-seq revealed that AEA caused an increased expression of the nuclear receptors NR4A1 and NR4A2. Knockdown of these receptors blocked the AEA-mediated anti-inflammatory effect. Conversely, NR4A agonists (CsnB, C-DIM12) also attenuated inflammatory gene expression. Microscale thermophoresis, NMR-spectroscopy, and Gal4 reporter gene assays confirmed the binding of AEA to NR4A. Moreover, AEA caused an NR4A-dependent recruitment of the nuclear corepressor NCoR1 to the CCL2 promotor. Finally, AEA also elicited anti-inflammatory effects in the vascular organ culture of mice, which was not observed after the genetic deletion of NR4A1 or NR4A2.AEA elicits a specific anti-inflammatory response in vascular smooth muscle cells through activation of NR4A. AEA analogous with high potential to bind NR4A receptors might act as novel anti-inflammatory drugs.
Fil: Teichmann, Tom. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research ; Alemania
Fil: Pflüger Mülle, Beatrice. German Centre of Cardiovascular Research ; Alemania. Goethe Universitat Frankfurt; Alemania
Fil: Martín Giménez, Virna Margarita. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Catolica de Cuyo - Sede San Juan. Facultad de Ciencias de la Alimentación, Bioquímicas y Farmacéuticas. Instituto de Investigación en Ciencias Químicas; Argentina
Fil: Sailer, Fiona. Goethe Universitat Frankfurt; Alemania
Fil: Dirks, Henrik. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research ; Alemania
Fil: Zehr, Simonida. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research ; Alemania
Fil: Warwick, Timothy. German Centre of Cardiovascular Research ; Alemania. Goethe Universitat Frankfurt; Alemania
Fil: Brettner, Felix. Goethe Universitat Frankfurt; Alemania
Fil: Munoz Tello, Paola. Vanderbilt University; Estados Unidos
Fil: Zimmer, Andreas. Universitat Bonn; Alemania
Fil: Tegeder, Irmgard. Goethe Universitat Frankfurt; Alemania
Fil: Thomas, Dominique. Goethe Universitat Frankfurt; Alemania. Fraunhofer Institute for Translational Medicine and Pharmacology; Alemania
Fil: Gurke, Robert. Fraunhofer Institute for Translational Medicine and Pharmacology; Alemania. Goethe Universitat Frankfurt; Alemania
Fil: Günther, Stefan. Max Plank-Institute for Heart and Lung Research ; Alemania
Fil: Heering, Jan. Fraunhofer Institute for Translational Medicine and Pharmacology; Alemania
Fil: Proschak, Ewgenij. Fraunhofer Institute for Translational Medicine and Pharmacology; Alemania. Goethe Universitat Frankfurt; Alemania
Fil: Geisslinger, Gerd. Goethe Universitat Frankfurt; Alemania
Fil: Bibli, Iris S.. German Centre of Cardiovascular Research; Alemania. Goethe Universitat Frankfurt; Alemania
Fil: Meyer zu Heringdorf, Dagmar. University Hospital Frankfurt. Institute of General Pharmacology and Toxicology; Alemania. Goethe Universitat Frankfurt; Alemania
Fil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Windbergs, Maike. Goethe Universitat Frankfurt; Alemania
Fil: Knapp, Stefan. Goethe Universitat Frankfurt; Alemania
Fil: Weigert, Andreas. Goethe Universitat Frankfurt; Alemania
Fil: Leisegang, Matthias S.. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research; Alemania
Fil: Kojetin, Douglas. Vanderbilt University; Estados Unidos
Fil: Brandes, Ralf P.. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research; Alemania
Materia
ANANDAMIDE
ANTIINFLAMMATORY EFFECTS
NR4A NUCLEAR RECEPTORS
ENDOCANNABINOIDS
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:11336/261401
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/261401
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling The endocannabinoid anandamide mediates anti‐inflammatory effects through activation of NR4A nuclear receptorsTeichmann, TomPflüger Mülle, BeatriceMartín Giménez, Virna MargaritaSailer, FionaDirks, HenrikZehr, SimonidaWarwick, TimothyBrettner, FelixMunoz Tello, PaolaZimmer, AndreasTegeder, IrmgardThomas, DominiqueGurke, RobertGünther, StefanHeering, JanProschak, EwgenijGeisslinger, GerdBibli, Iris S.Meyer zu Heringdorf, DagmarManucha, Walter Ariel FernandoWindbergs, MaikeKnapp, StefanWeigert, AndreasLeisegang, Matthias S.Kojetin, DouglasBrandes, Ralf P.ANANDAMIDEANTIINFLAMMATORY EFFECTSNR4A NUCLEAR RECEPTORSENDOCANNABINOIDShttps://purl.org/becyt/ford/3.4https://purl.org/becyt/ford/3Endocannabinoids are lipid mediators, which elicit complex biological effects that extend beyond the central nervous system. The tissue concentrations of endocannabinoids increase in atherosclerosis, and for the endocannabinoid N-arachidonoyl-ethanolamine (anandamide; AEA), this has been linked to a potential anti-inflammatory function. Focusing on vascular smooth muscle cells, we set out to determine the underlying mechanism. Confirming previous results, AEA pretreatment attenuated the cytokine-mediated induction of inflammatory gene expression like CCL2. Unexpectedly, this effect was also observed in preparations of cannabinoid receptor (CB) 1 and 2 knockout mice and after pertussis toxin treatment but was restricted to fairly high concentrations of the lipid. The anti-inflammatory effect of AEA required preincubation, suggesting an effect through gene induction. RNA-seq revealed that AEA caused an increased expression of the nuclear receptors NR4A1 and NR4A2. Knockdown of these receptors blocked the AEA-mediated anti-inflammatory effect. Conversely, NR4A agonists (CsnB, C-DIM12) also attenuated inflammatory gene expression. Microscale thermophoresis, NMR-spectroscopy, and Gal4 reporter gene assays confirmed the binding of AEA to NR4A. Moreover, AEA caused an NR4A-dependent recruitment of the nuclear corepressor NCoR1 to the CCL2 promotor. Finally, AEA also elicited anti-inflammatory effects in the vascular organ culture of mice, which was not observed after the genetic deletion of NR4A1 or NR4A2.AEA elicits a specific anti-inflammatory response in vascular smooth muscle cells through activation of NR4A. AEA analogous with high potential to bind NR4A receptors might act as novel anti-inflammatory drugs.Fil: Teichmann, Tom. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research ; AlemaniaFil: Pflüger Mülle, Beatrice. German Centre of Cardiovascular Research ; Alemania. Goethe Universitat Frankfurt; AlemaniaFil: Martín Giménez, Virna Margarita. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Catolica de Cuyo - Sede San Juan. Facultad de Ciencias de la Alimentación, Bioquímicas y Farmacéuticas. Instituto de Investigación en Ciencias Químicas; ArgentinaFil: Sailer, Fiona. Goethe Universitat Frankfurt; AlemaniaFil: Dirks, Henrik. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research ; AlemaniaFil: Zehr, Simonida. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research ; AlemaniaFil: Warwick, Timothy. German Centre of Cardiovascular Research ; Alemania. Goethe Universitat Frankfurt; AlemaniaFil: Brettner, Felix. Goethe Universitat Frankfurt; AlemaniaFil: Munoz Tello, Paola. Vanderbilt University; Estados UnidosFil: Zimmer, Andreas. Universitat Bonn; AlemaniaFil: Tegeder, Irmgard. Goethe Universitat Frankfurt; AlemaniaFil: Thomas, Dominique. Goethe Universitat Frankfurt; Alemania. Fraunhofer Institute for Translational Medicine and Pharmacology; AlemaniaFil: Gurke, Robert. Fraunhofer Institute for Translational Medicine and Pharmacology; Alemania. Goethe Universitat Frankfurt; AlemaniaFil: Günther, Stefan. Max Plank-Institute for Heart and Lung Research ; AlemaniaFil: Heering, Jan. Fraunhofer Institute for Translational Medicine and Pharmacology; AlemaniaFil: Proschak, Ewgenij. Fraunhofer Institute for Translational Medicine and Pharmacology; Alemania. Goethe Universitat Frankfurt; AlemaniaFil: Geisslinger, Gerd. Goethe Universitat Frankfurt; AlemaniaFil: Bibli, Iris S.. German Centre of Cardiovascular Research; Alemania. Goethe Universitat Frankfurt; AlemaniaFil: Meyer zu Heringdorf, Dagmar. University Hospital Frankfurt. Institute of General Pharmacology and Toxicology; Alemania. Goethe Universitat Frankfurt; AlemaniaFil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; ArgentinaFil: Windbergs, Maike. Goethe Universitat Frankfurt; AlemaniaFil: Knapp, Stefan. Goethe Universitat Frankfurt; AlemaniaFil: Weigert, Andreas. Goethe Universitat Frankfurt; AlemaniaFil: Leisegang, Matthias S.. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research; AlemaniaFil: Kojetin, Douglas. Vanderbilt University; Estados UnidosFil: Brandes, Ralf P.. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research; AlemaniaWiley Blackwell Publishing, Inc2024-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/261401Teichmann, Tom; Pflüger Mülle, Beatrice; Martín Giménez, Virna Margarita; Sailer, Fiona; Dirks, Henrik; et al.; The endocannabinoid anandamide mediates anti‐inflammatory effects through activation of NR4A nuclear receptors; Wiley Blackwell Publishing, Inc; British Journal of Pharmacology; 182; 5; 11-2024; 1164-11820007-1188CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://bpspubs.onlinelibrary.wiley.com/doi/10.1111/bph.17366info:eu-repo/semantics/altIdentifier/doi/10.1111/bph.17366info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:06:54Zoai:ri.conicet.gov.ar:11336/261401instacron: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:34982025-09-03 10:06:54.463CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv The endocannabinoid anandamide mediates anti‐inflammatory effects through activation of NR4A nuclear receptors
title The endocannabinoid anandamide mediates anti‐inflammatory effects through activation of NR4A nuclear receptors
spellingShingle The endocannabinoid anandamide mediates anti‐inflammatory effects through activation of NR4A nuclear receptors
Teichmann, Tom
ANANDAMIDE
ANTIINFLAMMATORY EFFECTS
NR4A NUCLEAR RECEPTORS
ENDOCANNABINOIDS
title_short The endocannabinoid anandamide mediates anti‐inflammatory effects through activation of NR4A nuclear receptors
title_full The endocannabinoid anandamide mediates anti‐inflammatory effects through activation of NR4A nuclear receptors
title_fullStr The endocannabinoid anandamide mediates anti‐inflammatory effects through activation of NR4A nuclear receptors
title_full_unstemmed The endocannabinoid anandamide mediates anti‐inflammatory effects through activation of NR4A nuclear receptors
title_sort The endocannabinoid anandamide mediates anti‐inflammatory effects through activation of NR4A nuclear receptors
dc.creator.none.fl_str_mv Teichmann, Tom
Pflüger Mülle, Beatrice
Martín Giménez, Virna Margarita
Sailer, Fiona
Dirks, Henrik
Zehr, Simonida
Warwick, Timothy
Brettner, Felix
Munoz Tello, Paola
Zimmer, Andreas
Tegeder, Irmgard
Thomas, Dominique
Gurke, Robert
Günther, Stefan
Heering, Jan
Proschak, Ewgenij
Geisslinger, Gerd
Bibli, Iris S.
Meyer zu Heringdorf, Dagmar
Manucha, Walter Ariel Fernando
Windbergs, Maike
Knapp, Stefan
Weigert, Andreas
Leisegang, Matthias S.
Kojetin, Douglas
Brandes, Ralf P.
author Teichmann, Tom
author_facet Teichmann, Tom
Pflüger Mülle, Beatrice
Martín Giménez, Virna Margarita
Sailer, Fiona
Dirks, Henrik
Zehr, Simonida
Warwick, Timothy
Brettner, Felix
Munoz Tello, Paola
Zimmer, Andreas
Tegeder, Irmgard
Thomas, Dominique
Gurke, Robert
Günther, Stefan
Heering, Jan
Proschak, Ewgenij
Geisslinger, Gerd
Bibli, Iris S.
Meyer zu Heringdorf, Dagmar
Manucha, Walter Ariel Fernando
Windbergs, Maike
Knapp, Stefan
Weigert, Andreas
Leisegang, Matthias S.
Kojetin, Douglas
Brandes, Ralf P.
author_role author
author2 Pflüger Mülle, Beatrice
Martín Giménez, Virna Margarita
Sailer, Fiona
Dirks, Henrik
Zehr, Simonida
Warwick, Timothy
Brettner, Felix
Munoz Tello, Paola
Zimmer, Andreas
Tegeder, Irmgard
Thomas, Dominique
Gurke, Robert
Günther, Stefan
Heering, Jan
Proschak, Ewgenij
Geisslinger, Gerd
Bibli, Iris S.
Meyer zu Heringdorf, Dagmar
Manucha, Walter Ariel Fernando
Windbergs, Maike
Knapp, Stefan
Weigert, Andreas
Leisegang, Matthias S.
Kojetin, Douglas
Brandes, Ralf P.
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv ANANDAMIDE
ANTIINFLAMMATORY EFFECTS
NR4A NUCLEAR RECEPTORS
ENDOCANNABINOIDS
topic ANANDAMIDE
ANTIINFLAMMATORY EFFECTS
NR4A NUCLEAR RECEPTORS
ENDOCANNABINOIDS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.4
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Endocannabinoids are lipid mediators, which elicit complex biological effects that extend beyond the central nervous system. The tissue concentrations of endocannabinoids increase in atherosclerosis, and for the endocannabinoid N-arachidonoyl-ethanolamine (anandamide; AEA), this has been linked to a potential anti-inflammatory function. Focusing on vascular smooth muscle cells, we set out to determine the underlying mechanism. Confirming previous results, AEA pretreatment attenuated the cytokine-mediated induction of inflammatory gene expression like CCL2. Unexpectedly, this effect was also observed in preparations of cannabinoid receptor (CB) 1 and 2 knockout mice and after pertussis toxin treatment but was restricted to fairly high concentrations of the lipid. The anti-inflammatory effect of AEA required preincubation, suggesting an effect through gene induction. RNA-seq revealed that AEA caused an increased expression of the nuclear receptors NR4A1 and NR4A2. Knockdown of these receptors blocked the AEA-mediated anti-inflammatory effect. Conversely, NR4A agonists (CsnB, C-DIM12) also attenuated inflammatory gene expression. Microscale thermophoresis, NMR-spectroscopy, and Gal4 reporter gene assays confirmed the binding of AEA to NR4A. Moreover, AEA caused an NR4A-dependent recruitment of the nuclear corepressor NCoR1 to the CCL2 promotor. Finally, AEA also elicited anti-inflammatory effects in the vascular organ culture of mice, which was not observed after the genetic deletion of NR4A1 or NR4A2.AEA elicits a specific anti-inflammatory response in vascular smooth muscle cells through activation of NR4A. AEA analogous with high potential to bind NR4A receptors might act as novel anti-inflammatory drugs.
Fil: Teichmann, Tom. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research ; Alemania
Fil: Pflüger Mülle, Beatrice. German Centre of Cardiovascular Research ; Alemania. Goethe Universitat Frankfurt; Alemania
Fil: Martín Giménez, Virna Margarita. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Catolica de Cuyo - Sede San Juan. Facultad de Ciencias de la Alimentación, Bioquímicas y Farmacéuticas. Instituto de Investigación en Ciencias Químicas; Argentina
Fil: Sailer, Fiona. Goethe Universitat Frankfurt; Alemania
Fil: Dirks, Henrik. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research ; Alemania
Fil: Zehr, Simonida. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research ; Alemania
Fil: Warwick, Timothy. German Centre of Cardiovascular Research ; Alemania. Goethe Universitat Frankfurt; Alemania
Fil: Brettner, Felix. Goethe Universitat Frankfurt; Alemania
Fil: Munoz Tello, Paola. Vanderbilt University; Estados Unidos
Fil: Zimmer, Andreas. Universitat Bonn; Alemania
Fil: Tegeder, Irmgard. Goethe Universitat Frankfurt; Alemania
Fil: Thomas, Dominique. Goethe Universitat Frankfurt; Alemania. Fraunhofer Institute for Translational Medicine and Pharmacology; Alemania
Fil: Gurke, Robert. Fraunhofer Institute for Translational Medicine and Pharmacology; Alemania. Goethe Universitat Frankfurt; Alemania
Fil: Günther, Stefan. Max Plank-Institute for Heart and Lung Research ; Alemania
Fil: Heering, Jan. Fraunhofer Institute for Translational Medicine and Pharmacology; Alemania
Fil: Proschak, Ewgenij. Fraunhofer Institute for Translational Medicine and Pharmacology; Alemania. Goethe Universitat Frankfurt; Alemania
Fil: Geisslinger, Gerd. Goethe Universitat Frankfurt; Alemania
Fil: Bibli, Iris S.. German Centre of Cardiovascular Research; Alemania. Goethe Universitat Frankfurt; Alemania
Fil: Meyer zu Heringdorf, Dagmar. University Hospital Frankfurt. Institute of General Pharmacology and Toxicology; Alemania. Goethe Universitat Frankfurt; Alemania
Fil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Windbergs, Maike. Goethe Universitat Frankfurt; Alemania
Fil: Knapp, Stefan. Goethe Universitat Frankfurt; Alemania
Fil: Weigert, Andreas. Goethe Universitat Frankfurt; Alemania
Fil: Leisegang, Matthias S.. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research; Alemania
Fil: Kojetin, Douglas. Vanderbilt University; Estados Unidos
Fil: Brandes, Ralf P.. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research; Alemania
description Endocannabinoids are lipid mediators, which elicit complex biological effects that extend beyond the central nervous system. The tissue concentrations of endocannabinoids increase in atherosclerosis, and for the endocannabinoid N-arachidonoyl-ethanolamine (anandamide; AEA), this has been linked to a potential anti-inflammatory function. Focusing on vascular smooth muscle cells, we set out to determine the underlying mechanism. Confirming previous results, AEA pretreatment attenuated the cytokine-mediated induction of inflammatory gene expression like CCL2. Unexpectedly, this effect was also observed in preparations of cannabinoid receptor (CB) 1 and 2 knockout mice and after pertussis toxin treatment but was restricted to fairly high concentrations of the lipid. The anti-inflammatory effect of AEA required preincubation, suggesting an effect through gene induction. RNA-seq revealed that AEA caused an increased expression of the nuclear receptors NR4A1 and NR4A2. Knockdown of these receptors blocked the AEA-mediated anti-inflammatory effect. Conversely, NR4A agonists (CsnB, C-DIM12) also attenuated inflammatory gene expression. Microscale thermophoresis, NMR-spectroscopy, and Gal4 reporter gene assays confirmed the binding of AEA to NR4A. Moreover, AEA caused an NR4A-dependent recruitment of the nuclear corepressor NCoR1 to the CCL2 promotor. Finally, AEA also elicited anti-inflammatory effects in the vascular organ culture of mice, which was not observed after the genetic deletion of NR4A1 or NR4A2.AEA elicits a specific anti-inflammatory response in vascular smooth muscle cells through activation of NR4A. AEA analogous with high potential to bind NR4A receptors might act as novel anti-inflammatory drugs.
publishDate 2024
dc.date.none.fl_str_mv 2024-11
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/11336/261401
Teichmann, Tom; Pflüger Mülle, Beatrice; Martín Giménez, Virna Margarita; Sailer, Fiona; Dirks, Henrik; et al.; The endocannabinoid anandamide mediates anti‐inflammatory effects through activation of NR4A nuclear receptors; Wiley Blackwell Publishing, Inc; British Journal of Pharmacology; 182; 5; 11-2024; 1164-1182
0007-1188
CONICET Digital
CONICET
url http://hdl.handle.net/11336/261401
identifier_str_mv Teichmann, Tom; Pflüger Mülle, Beatrice; Martín Giménez, Virna Margarita; Sailer, Fiona; Dirks, Henrik; et al.; The endocannabinoid anandamide mediates anti‐inflammatory effects through activation of NR4A nuclear receptors; Wiley Blackwell Publishing, Inc; British Journal of Pharmacology; 182; 5; 11-2024; 1164-1182
0007-1188
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://bpspubs.onlinelibrary.wiley.com/doi/10.1111/bph.17366
info:eu-repo/semantics/altIdentifier/doi/10.1111/bph.17366
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
application/pdf
dc.publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
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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