M1 macrophage polarization is dependent on TRPC1-mediated calcium entry

Autores
Chauhan, Arun; Sun, Yuyang; Sukumaran, Pramod; Quenum Zangbede, Fredice O.; Jondle, Christopher N.; Sharma, Atul; Evans, Dustin L.; Chauhan, Pooja; Szlabick, Randolph E.; Aaland, Mary O.; Birnbaumer, Lutz; Sharma, Jyotika; Singh, Brij B.; Mishra, Bibhuti B.
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Fil: Chauhan, Arun. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Sun, Yuyang. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Sukumaran, Pramod. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Quenum Zangbede, Fredice O. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Jondle, Christopher N. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Sharma, Atul. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Evans, Dustin L. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Chauhan, Pooja. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Szlabick, Randolph E. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Aaland, Mary O. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentina
Fil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Birnbaumer, Lutz. Research Triangle Park. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados Unidos
Fil Sharma, Jyotika. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Singh, Brij B. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Mishra, Bibhuti B. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Abstract: Macrophage plasticity is essential for innate immunity, but in-depth signaling mechanism(s) regulating their functional phenotypes are ill-defined. Here we report that interferon (IFN) γ priming of naive macrophages induces store-mediated Ca2+ entry and inhibition of Ca2+ entry impairs polarization to M1 inflammatory phenotype. In vitro and in vivo functional analyses revealed ORAI1 to be a primary contributor to basal Ca2+ influx in macrophages, whereas IFNγ-induced Ca2+ influx was mediated by TRPC1. Deficiency of TRPC1 displayed abrogated IFNγ-induced M1 inflammatory mediators in macrophages. In a preclinical model of peritonitis by Klebsiella pneumoniae infection, macrophages showed increased Ca2+ influx, which was TRPC1 dependent. Macrophages from infected TRPC1-/- mice showed inhibited expression of M1-associated signature molecules. Furthermore, in human patients with systemic inflammatory response syndrome, the level of TRPC1 expression in circulating macrophages directly correlated with M1 inflammatory mediators. Overall, TRPC1-mediated Ca2+ influx is essential for the induction/shaping of macrophage polarization to M1 inflammatory phenotype.
Fuente
iScience. 2018;8:85-102
Materia
INMUNOLOGIA
SISTEMA INMUNOLOGICO
CALCIO
SEPSIS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
Repositorio Institucional (UCA)
Institución
Pontificia Universidad Católica Argentina
OAI Identificador
oai:ucacris:123456789/8685

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oai_identifier_str oai:ucacris:123456789/8685
network_acronym_str RIUCA
repository_id_str 2585
network_name_str Repositorio Institucional (UCA)
spelling M1 macrophage polarization is dependent on TRPC1-mediated calcium entryChauhan, ArunSun, YuyangSukumaran, PramodQuenum Zangbede, Fredice O.Jondle, Christopher N.Sharma, AtulEvans, Dustin L.Chauhan, PoojaSzlabick, Randolph E.Aaland, Mary O.Birnbaumer, LutzSharma, JyotikaSingh, Brij B.Mishra, Bibhuti B.INMUNOLOGIASISTEMA INMUNOLOGICOCALCIOSEPSISFil: Chauhan, Arun. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United StatesFil: Sun, Yuyang. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United StatesFil: Sukumaran, Pramod. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United StatesFil: Quenum Zangbede, Fredice O. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United StatesFil: Jondle, Christopher N. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United StatesFil: Sharma, Atul. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United StatesFil: Evans, Dustin L. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United StatesFil: Chauhan, Pooja. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United StatesFil: Szlabick, Randolph E. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United StatesFil: Aaland, Mary O. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United StatesFil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; ArgentinaFil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Birnbaumer, Lutz. Research Triangle Park. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados UnidosFil Sharma, Jyotika. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United StatesFil: Singh, Brij B. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United StatesFil: Mishra, Bibhuti B. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United StatesAbstract: Macrophage plasticity is essential for innate immunity, but in-depth signaling mechanism(s) regulating their functional phenotypes are ill-defined. Here we report that interferon (IFN) γ priming of naive macrophages induces store-mediated Ca2+ entry and inhibition of Ca2+ entry impairs polarization to M1 inflammatory phenotype. In vitro and in vivo functional analyses revealed ORAI1 to be a primary contributor to basal Ca2+ influx in macrophages, whereas IFNγ-induced Ca2+ influx was mediated by TRPC1. Deficiency of TRPC1 displayed abrogated IFNγ-induced M1 inflammatory mediators in macrophages. In a preclinical model of peritonitis by Klebsiella pneumoniae infection, macrophages showed increased Ca2+ influx, which was TRPC1 dependent. Macrophages from infected TRPC1-/- mice showed inhibited expression of M1-associated signature molecules. Furthermore, in human patients with systemic inflammatory response syndrome, the level of TRPC1 expression in circulating macrophages directly correlated with M1 inflammatory mediators. Overall, TRPC1-mediated Ca2+ influx is essential for the induction/shaping of macrophage polarization to M1 inflammatory phenotype.Elsevier (Cell Press)2018info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://repositorio.uca.edu.ar/handle/123456789/86852589-004210.1016/j.isci.2018.09.01430293012Chauhan A, Sun Y, Sukumaran P, et al. M1 macrophage polarization is dependent on TRPC1-mediated calcium entry. iScience. 2018;8:85-102. doi:10.1016/j.isci.2018.09.014 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8685iScience. 2018;8:85-102reponame:Repositorio Institucional (UCA)instname:Pontificia Universidad Católica Argentinaenginfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/4.0/2025-07-03T10:56:54Zoai:ucacris:123456789/8685instacron:UCAInstitucionalhttps://repositorio.uca.edu.ar/Universidad privadaNo correspondehttps://repositorio.uca.edu.ar/oaiclaudia_fernandez@uca.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:25852025-07-03 10:56:55.008Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentinafalse
dc.title.none.fl_str_mv M1 macrophage polarization is dependent on TRPC1-mediated calcium entry
title M1 macrophage polarization is dependent on TRPC1-mediated calcium entry
spellingShingle M1 macrophage polarization is dependent on TRPC1-mediated calcium entry
Chauhan, Arun
INMUNOLOGIA
SISTEMA INMUNOLOGICO
CALCIO
SEPSIS
title_short M1 macrophage polarization is dependent on TRPC1-mediated calcium entry
title_full M1 macrophage polarization is dependent on TRPC1-mediated calcium entry
title_fullStr M1 macrophage polarization is dependent on TRPC1-mediated calcium entry
title_full_unstemmed M1 macrophage polarization is dependent on TRPC1-mediated calcium entry
title_sort M1 macrophage polarization is dependent on TRPC1-mediated calcium entry
dc.creator.none.fl_str_mv Chauhan, Arun
Sun, Yuyang
Sukumaran, Pramod
Quenum Zangbede, Fredice O.
Jondle, Christopher N.
Sharma, Atul
Evans, Dustin L.
Chauhan, Pooja
Szlabick, Randolph E.
Aaland, Mary O.
Birnbaumer, Lutz
Sharma, Jyotika
Singh, Brij B.
Mishra, Bibhuti B.
author Chauhan, Arun
author_facet Chauhan, Arun
Sun, Yuyang
Sukumaran, Pramod
Quenum Zangbede, Fredice O.
Jondle, Christopher N.
Sharma, Atul
Evans, Dustin L.
Chauhan, Pooja
Szlabick, Randolph E.
Aaland, Mary O.
Birnbaumer, Lutz
Sharma, Jyotika
Singh, Brij B.
Mishra, Bibhuti B.
author_role author
author2 Sun, Yuyang
Sukumaran, Pramod
Quenum Zangbede, Fredice O.
Jondle, Christopher N.
Sharma, Atul
Evans, Dustin L.
Chauhan, Pooja
Szlabick, Randolph E.
Aaland, Mary O.
Birnbaumer, Lutz
Sharma, Jyotika
Singh, Brij B.
Mishra, Bibhuti B.
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv INMUNOLOGIA
SISTEMA INMUNOLOGICO
CALCIO
SEPSIS
topic INMUNOLOGIA
SISTEMA INMUNOLOGICO
CALCIO
SEPSIS
dc.description.none.fl_txt_mv Fil: Chauhan, Arun. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Sun, Yuyang. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Sukumaran, Pramod. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Quenum Zangbede, Fredice O. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Jondle, Christopher N. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Sharma, Atul. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Evans, Dustin L. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Chauhan, Pooja. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Szlabick, Randolph E. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Aaland, Mary O. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentina
Fil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Birnbaumer, Lutz. Research Triangle Park. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados Unidos
Fil Sharma, Jyotika. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Singh, Brij B. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Fil: Mishra, Bibhuti B. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
Abstract: Macrophage plasticity is essential for innate immunity, but in-depth signaling mechanism(s) regulating their functional phenotypes are ill-defined. Here we report that interferon (IFN) γ priming of naive macrophages induces store-mediated Ca2+ entry and inhibition of Ca2+ entry impairs polarization to M1 inflammatory phenotype. In vitro and in vivo functional analyses revealed ORAI1 to be a primary contributor to basal Ca2+ influx in macrophages, whereas IFNγ-induced Ca2+ influx was mediated by TRPC1. Deficiency of TRPC1 displayed abrogated IFNγ-induced M1 inflammatory mediators in macrophages. In a preclinical model of peritonitis by Klebsiella pneumoniae infection, macrophages showed increased Ca2+ influx, which was TRPC1 dependent. Macrophages from infected TRPC1-/- mice showed inhibited expression of M1-associated signature molecules. Furthermore, in human patients with systemic inflammatory response syndrome, the level of TRPC1 expression in circulating macrophages directly correlated with M1 inflammatory mediators. Overall, TRPC1-mediated Ca2+ influx is essential for the induction/shaping of macrophage polarization to M1 inflammatory phenotype.
description Fil: Chauhan, Arun. The University of North Dakota. School of Medicine & Health Sciences. Department of Biomedical Sciences and Department of Surgery; United States
publishDate 2018
dc.date.none.fl_str_mv 2018
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 https://repositorio.uca.edu.ar/handle/123456789/8685
2589-0042
10.1016/j.isci.2018.09.014
30293012
Chauhan A, Sun Y, Sukumaran P, et al. M1 macrophage polarization is dependent on TRPC1-mediated calcium entry. iScience. 2018;8:85-102. doi:10.1016/j.isci.2018.09.014 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8685
url https://repositorio.uca.edu.ar/handle/123456789/8685
identifier_str_mv 2589-0042
10.1016/j.isci.2018.09.014
30293012
Chauhan A, Sun Y, Sukumaran P, et al. M1 macrophage polarization is dependent on TRPC1-mediated calcium entry. iScience. 2018;8:85-102. doi:10.1016/j.isci.2018.09.014 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8685
dc.language.none.fl_str_mv eng
language eng
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/4.0/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/4.0/
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Elsevier (Cell Press)
publisher.none.fl_str_mv Elsevier (Cell Press)
dc.source.none.fl_str_mv iScience. 2018;8:85-102
reponame:Repositorio Institucional (UCA)
instname:Pontificia Universidad Católica Argentina
reponame_str Repositorio Institucional (UCA)
collection Repositorio Institucional (UCA)
instname_str Pontificia Universidad Católica Argentina
repository.name.fl_str_mv Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentina
repository.mail.fl_str_mv claudia_fernandez@uca.edu.ar
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score 13.22299