Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3

Autores
Kumarasamy, Sivarajan; Solanki, Sumeet; Atolagbe, Oluwatomisin T.; Joe, Bina; Birnbaumer, Lutz; Vazquez, Guillermo
Año de publicación
2017
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
In previous studies using mice with macrophage-specific loss of TRPC3 we found a significant, selective effect of TRPC3 on the biology of M1, or inflammatory macrophages. Whereas activation of some components of the unfolded protein response and the pro-apoptotic mediators CamkII and Stat1 was impaired in Trpc3-deficient M1 cells, gathering insight about other molecular signatures within macrophages that might be affected by Trpc3 expression requires an alternative approach. In the present study we conducted RNA-seq analysis to interrogate the transcriptome of M1 macrophages derived from mice with macrophage-specific loss of TRPC3 and their littermate controls. We identified 160 significantly differentially expressed genes between the two groups, of which 62 were upregulated and 98 downregulated in control vs. Trpc3-deficient M1 macrophages. Gene ontology analysis revealed enrichment in processes associated to cellular movement and lipid signaling, whereas the enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways included networks for calcium signaling and cell adhesion molecules, among others. This is the first deep transcriptomic analysis of macrophages in the context of Trpc3 deficiency and the data presented constitutes a unique resource to further explore functions of TRPC3 in macrophage biology.
Fil: Kumarasamy, Sivarajan. University of Toledo; Estados Unidos
Fil: Solanki, Sumeet. University of Toledo; Estados Unidos
Fil: Atolagbe, Oluwatomisin T.. University of Toledo; Estados Unidos
Fil: Joe, Bina. University of Toledo; Estados Unidos
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
Fil: Vazquez, Guillermo. University of Toledo; Estados Unidos
Materia
TRPC3
M1 Macrophages
RNA
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/47679

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spelling Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3Kumarasamy, SivarajanSolanki, SumeetAtolagbe, Oluwatomisin T.Joe, BinaBirnbaumer, LutzVazquez, GuillermoTRPC3M1 MacrophagesRNAhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3In previous studies using mice with macrophage-specific loss of TRPC3 we found a significant, selective effect of TRPC3 on the biology of M1, or inflammatory macrophages. Whereas activation of some components of the unfolded protein response and the pro-apoptotic mediators CamkII and Stat1 was impaired in Trpc3-deficient M1 cells, gathering insight about other molecular signatures within macrophages that might be affected by Trpc3 expression requires an alternative approach. In the present study we conducted RNA-seq analysis to interrogate the transcriptome of M1 macrophages derived from mice with macrophage-specific loss of TRPC3 and their littermate controls. We identified 160 significantly differentially expressed genes between the two groups, of which 62 were upregulated and 98 downregulated in control vs. Trpc3-deficient M1 macrophages. Gene ontology analysis revealed enrichment in processes associated to cellular movement and lipid signaling, whereas the enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways included networks for calcium signaling and cell adhesion molecules, among others. This is the first deep transcriptomic analysis of macrophages in the context of Trpc3 deficiency and the data presented constitutes a unique resource to further explore functions of TRPC3 in macrophage biology.Fil: Kumarasamy, Sivarajan. University of Toledo; Estados UnidosFil: Solanki, Sumeet. University of Toledo; Estados UnidosFil: Atolagbe, Oluwatomisin T.. University of Toledo; Estados UnidosFil: Joe, Bina. University of Toledo; Estados UnidosFil: 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; ArgentinaFil: Vazquez, Guillermo. University of Toledo; Estados UnidosNature Publishing Group2017-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/47679Kumarasamy, Sivarajan; Solanki, Sumeet; Atolagbe, Oluwatomisin T.; Joe, Bina; Birnbaumer, Lutz; et al.; Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3; Nature Publishing Group; Scientific Reports; 7; 1-2017; 1-62045-2322CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1038/srep39867info:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/srep39867info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:56:06Zoai:ri.conicet.gov.ar:11336/47679instacron: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 09:56:06.641CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3
title Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3
spellingShingle Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3
Kumarasamy, Sivarajan
TRPC3
M1 Macrophages
RNA
title_short Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3
title_full Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3
title_fullStr Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3
title_full_unstemmed Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3
title_sort Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3
dc.creator.none.fl_str_mv Kumarasamy, Sivarajan
Solanki, Sumeet
Atolagbe, Oluwatomisin T.
Joe, Bina
Birnbaumer, Lutz
Vazquez, Guillermo
author Kumarasamy, Sivarajan
author_facet Kumarasamy, Sivarajan
Solanki, Sumeet
Atolagbe, Oluwatomisin T.
Joe, Bina
Birnbaumer, Lutz
Vazquez, Guillermo
author_role author
author2 Solanki, Sumeet
Atolagbe, Oluwatomisin T.
Joe, Bina
Birnbaumer, Lutz
Vazquez, Guillermo
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv TRPC3
M1 Macrophages
RNA
topic TRPC3
M1 Macrophages
RNA
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv In previous studies using mice with macrophage-specific loss of TRPC3 we found a significant, selective effect of TRPC3 on the biology of M1, or inflammatory macrophages. Whereas activation of some components of the unfolded protein response and the pro-apoptotic mediators CamkII and Stat1 was impaired in Trpc3-deficient M1 cells, gathering insight about other molecular signatures within macrophages that might be affected by Trpc3 expression requires an alternative approach. In the present study we conducted RNA-seq analysis to interrogate the transcriptome of M1 macrophages derived from mice with macrophage-specific loss of TRPC3 and their littermate controls. We identified 160 significantly differentially expressed genes between the two groups, of which 62 were upregulated and 98 downregulated in control vs. Trpc3-deficient M1 macrophages. Gene ontology analysis revealed enrichment in processes associated to cellular movement and lipid signaling, whereas the enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways included networks for calcium signaling and cell adhesion molecules, among others. This is the first deep transcriptomic analysis of macrophages in the context of Trpc3 deficiency and the data presented constitutes a unique resource to further explore functions of TRPC3 in macrophage biology.
Fil: Kumarasamy, Sivarajan. University of Toledo; Estados Unidos
Fil: Solanki, Sumeet. University of Toledo; Estados Unidos
Fil: Atolagbe, Oluwatomisin T.. University of Toledo; Estados Unidos
Fil: Joe, Bina. University of Toledo; Estados Unidos
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
Fil: Vazquez, Guillermo. University of Toledo; Estados Unidos
description In previous studies using mice with macrophage-specific loss of TRPC3 we found a significant, selective effect of TRPC3 on the biology of M1, or inflammatory macrophages. Whereas activation of some components of the unfolded protein response and the pro-apoptotic mediators CamkII and Stat1 was impaired in Trpc3-deficient M1 cells, gathering insight about other molecular signatures within macrophages that might be affected by Trpc3 expression requires an alternative approach. In the present study we conducted RNA-seq analysis to interrogate the transcriptome of M1 macrophages derived from mice with macrophage-specific loss of TRPC3 and their littermate controls. We identified 160 significantly differentially expressed genes between the two groups, of which 62 were upregulated and 98 downregulated in control vs. Trpc3-deficient M1 macrophages. Gene ontology analysis revealed enrichment in processes associated to cellular movement and lipid signaling, whereas the enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways included networks for calcium signaling and cell adhesion molecules, among others. This is the first deep transcriptomic analysis of macrophages in the context of Trpc3 deficiency and the data presented constitutes a unique resource to further explore functions of TRPC3 in macrophage biology.
publishDate 2017
dc.date.none.fl_str_mv 2017-01
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/11336/47679
Kumarasamy, Sivarajan; Solanki, Sumeet; Atolagbe, Oluwatomisin T.; Joe, Bina; Birnbaumer, Lutz; et al.; Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3; Nature Publishing Group; Scientific Reports; 7; 1-2017; 1-6
2045-2322
CONICET Digital
CONICET
url http://hdl.handle.net/11336/47679
identifier_str_mv Kumarasamy, Sivarajan; Solanki, Sumeet; Atolagbe, Oluwatomisin T.; Joe, Bina; Birnbaumer, Lutz; et al.; Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3; Nature Publishing Group; Scientific Reports; 7; 1-2017; 1-6
2045-2322
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1038/srep39867
info:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/srep39867
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Nature Publishing Group
publisher.none.fl_str_mv Nature Publishing Group
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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