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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/47679
Ver los metadatos del registro completo
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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 |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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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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