Mostrar el registro sencillo del ítem
dc.contributor.author
Chauhan, Arun
dc.contributor.author
Sun, Yuyang
dc.contributor.author
Sukumaran, Pramod
dc.contributor.author
Quenum Zangbede, Fredice O.
dc.contributor.author
Jondle, Christopher N.
dc.contributor.author
Sharma, Atul
dc.contributor.author
Evans, Dustin L.
dc.contributor.author
Chauhan, Pooja
dc.contributor.author
Szlabick, Randolph E.
dc.contributor.author
Aaland, Mary O.
dc.contributor.author
Birnbaumer, Lutz
dc.contributor.author
Sharma, Jyotika
dc.contributor.author
Singh, Brij B.
dc.contributor.author
Mishra, Bibhuti B.
dc.date.available
2020-03-12T21:03:37Z
dc.date.issued
2018-10
dc.identifier.citation
Chauhan, Arun; Sun, Yuyang; Sukumaran, Pramod; Quenum Zangbede, Fredice O.; Jondle, Christopher N.; et al.; M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry; Elsevier Inc.; iScience; 8; 10-2018; 85-102
dc.identifier.issn
2589-0042
dc.identifier.uri
http://hdl.handle.net/11336/99403
dc.description.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) g 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 IFNg-induced Ca2+ influx was mediated by TRPC1. Deficiency of TRPC1 displayed abrogated IFNg-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.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier Inc.
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.subject
BIOLOGICAL SCIENCES
dc.subject
IMMUNE RESPONSE
dc.subject
IMMUNOLOGY
dc.subject.classification
Biología Celular, Microbiología
dc.subject.classification
Ciencias Biológicas
dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
dc.title
M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-03-10T12:21:32Z
dc.journal.volume
8
dc.journal.pagination
85-102
dc.journal.pais
Estados Unidos
dc.description.fil
Fil: Chauhan, Arun. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Sun, Yuyang. Texas A&M University; Estados Unidos. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Sukumaran, Pramod. Texas A&M University; Estados Unidos. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Quenum Zangbede, Fredice O.. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Jondle, Christopher N.. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Sharma, Atul. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Evans, Dustin L.. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Chauhan, Pooja. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Szlabick, Randolph E.. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Aaland, Mary O.. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina. National Institutes of Health; Estados Unidos
dc.description.fil
Fil: Sharma, Jyotika. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Singh, Brij B.. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Mishra, Bibhuti B.. University of North Dakota; Estados Unidos
dc.journal.title
iScience
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.isci.2018.09.014
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S2589004218301494
Archivos asociados