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
- Institución
- Pontificia Universidad Católica Argentina
- OAI Identificador
- oai:ucacris:123456789/8685
Ver los metadatos del registro completo
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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) |
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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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13.22299 |