Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels

Autores
Camacho Londoño, Juan E.; Marx, André; Kraft, Axel E.; Schürger, Alexander; Richter, Christin; Dietrich, Alexander; Lipp, Peter; Birnbaumer, Lutz; Freichel, Marc
Año de publicación
2020
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
TRPC proteins form cation conducting channels regulated by different stimuli and are regulators of the cellular calcium homeostasis. TRPC are expressed in cardiac cells including cardiac fibroblasts (CFs) and have been implicated in the development of pathological cardiac remodeling including fibrosis. Using Ca2+ imaging and several compound TRPC knockout mouse lines we analyzed the involvement of TRPC proteins for the angiotensin II (AngII)-induced changes in Ca2+ homeostasis in CFs isolated from adult mice. Using qPCR we detected transcripts of all Trpc genes in CFs; Trpc1, Trpc3 and Trpc4 being the most abundant ones. We show that the AngII-induced Ca2+ entry but also Ca2+ release from intracellular stores are critically dependent on the density of CFs in culture and are inversely correlated with the expression of the myofibroblast marker α-smooth muscle actin. Our Ca2+ measurements depict that the AngII- and thrombin-induced Ca2+ transients, and the AngII-induced Ca2+ entry and Ca2+ release are not affected in CFs isolated from mice lacking all seven TRPC proteins (TRPC-hepta KO) compared to control cells. However, pre-incubation with GSK7975A (10 µM), which sufficiently inhibits CRAC channels in other cells, abolished AngII-induced Ca2+ entry. Consequently, we conclude the dispensability of the TRPC channels for the acute neurohumoral Ca2+ signaling evoked by AngII in isolated CFs and suggest the contribution of members of the Orai channel family as molecular constituents responsible for this pathophysiologically important Ca2+ entry pathway.
Fil: Camacho Londoño, Juan E.. Ruprecht Karls Universitat Heidelberg; Alemania
Fil: Marx, André. Ruprecht Karls Universitat Heidelberg; Alemania
Fil: Kraft, Axel E.. Ruprecht Karls Universitat Heidelberg; Alemania
Fil: Schürger, Alexander. Ruprecht Karls Universitat Heidelberg; Alemania
Fil: Richter, Christin. Ruprecht Karls Universitat Heidelberg; Alemania
Fil: Dietrich, Alexander. Ludwig Maximilians Universitat; Alemania
Fil: Lipp, Peter. Universitat Saarland; Alemania
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: Freichel, Marc. Ruprecht Karls Universitat Heidelberg; Alemania
Materia
ANGIOTENSIN II
CA2+ RELEASE AND CA2+ ENTRY
CARDIAC FIBROBLASTS (CFS)
TRPC CHANNELS
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:11336/141717
Acceder
id CONICETDig_9d20e8993fb3f283ffa70a709c97dd7a
oai_identifier_str oai:ri.conicet.gov.ar:11336/141717
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC ChannelsCamacho Londoño, Juan E.Marx, AndréKraft, Axel E.Schürger, AlexanderRichter, ChristinDietrich, AlexanderLipp, PeterBirnbaumer, LutzFreichel, MarcANGIOTENSIN IICA2+ RELEASE AND CA2+ ENTRYCARDIAC FIBROBLASTS (CFS)TRPC CHANNELShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1TRPC proteins form cation conducting channels regulated by different stimuli and are regulators of the cellular calcium homeostasis. TRPC are expressed in cardiac cells including cardiac fibroblasts (CFs) and have been implicated in the development of pathological cardiac remodeling including fibrosis. Using Ca2+ imaging and several compound TRPC knockout mouse lines we analyzed the involvement of TRPC proteins for the angiotensin II (AngII)-induced changes in Ca2+ homeostasis in CFs isolated from adult mice. Using qPCR we detected transcripts of all Trpc genes in CFs; Trpc1, Trpc3 and Trpc4 being the most abundant ones. We show that the AngII-induced Ca2+ entry but also Ca2+ release from intracellular stores are critically dependent on the density of CFs in culture and are inversely correlated with the expression of the myofibroblast marker α-smooth muscle actin. Our Ca2+ measurements depict that the AngII- and thrombin-induced Ca2+ transients, and the AngII-induced Ca2+ entry and Ca2+ release are not affected in CFs isolated from mice lacking all seven TRPC proteins (TRPC-hepta KO) compared to control cells. However, pre-incubation with GSK7975A (10 µM), which sufficiently inhibits CRAC channels in other cells, abolished AngII-induced Ca2+ entry. Consequently, we conclude the dispensability of the TRPC channels for the acute neurohumoral Ca2+ signaling evoked by AngII in isolated CFs and suggest the contribution of members of the Orai channel family as molecular constituents responsible for this pathophysiologically important Ca2+ entry pathway.Fil: Camacho Londoño, Juan E.. Ruprecht Karls Universitat Heidelberg; AlemaniaFil: Marx, André. Ruprecht Karls Universitat Heidelberg; AlemaniaFil: Kraft, Axel E.. Ruprecht Karls Universitat Heidelberg; AlemaniaFil: Schürger, Alexander. Ruprecht Karls Universitat Heidelberg; AlemaniaFil: Richter, Christin. Ruprecht Karls Universitat Heidelberg; AlemaniaFil: Dietrich, Alexander. Ludwig Maximilians Universitat; AlemaniaFil: Lipp, Peter. Universitat Saarland; AlemaniaFil: 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: Freichel, Marc. Ruprecht Karls Universitat Heidelberg; AlemaniaMolecular Diversity Preservation International2020-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/141717Camacho Londoño, Juan E.; Marx, André; Kraft, Axel E.; Schürger, Alexander; Richter, Christin; et al.; Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels; Molecular Diversity Preservation International; Cells; 9; 2; 1-2020; 1-272073-44092073-4409CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.3390/cells9020322info:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/2073-4409/9/2/322info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:58:44Zoai:ri.conicet.gov.ar:11336/141717instacron: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 09:58:44.963CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels
title Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels
spellingShingle Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels
Camacho Londoño, Juan E.
ANGIOTENSIN II
CA2+ RELEASE AND CA2+ ENTRY
CARDIAC FIBROBLASTS (CFS)
TRPC CHANNELS
title_short Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels
title_full Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels
title_fullStr Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels
title_full_unstemmed Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels
title_sort Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels
dc.creator.none.fl_str_mv Camacho Londoño, Juan E.
Marx, André
Kraft, Axel E.
Schürger, Alexander
Richter, Christin
Dietrich, Alexander
Lipp, Peter
Birnbaumer, Lutz
Freichel, Marc
author Camacho Londoño, Juan E.
author_facet Camacho Londoño, Juan E.
Marx, André
Kraft, Axel E.
Schürger, Alexander
Richter, Christin
Dietrich, Alexander
Lipp, Peter
Birnbaumer, Lutz
Freichel, Marc
author_role author
author2 Marx, André
Kraft, Axel E.
Schürger, Alexander
Richter, Christin
Dietrich, Alexander
Lipp, Peter
Birnbaumer, Lutz
Freichel, Marc
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv ANGIOTENSIN II
CA2+ RELEASE AND CA2+ ENTRY
CARDIAC FIBROBLASTS (CFS)
TRPC CHANNELS
topic ANGIOTENSIN II
CA2+ RELEASE AND CA2+ ENTRY
CARDIAC FIBROBLASTS (CFS)
TRPC CHANNELS
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv TRPC proteins form cation conducting channels regulated by different stimuli and are regulators of the cellular calcium homeostasis. TRPC are expressed in cardiac cells including cardiac fibroblasts (CFs) and have been implicated in the development of pathological cardiac remodeling including fibrosis. Using Ca2+ imaging and several compound TRPC knockout mouse lines we analyzed the involvement of TRPC proteins for the angiotensin II (AngII)-induced changes in Ca2+ homeostasis in CFs isolated from adult mice. Using qPCR we detected transcripts of all Trpc genes in CFs; Trpc1, Trpc3 and Trpc4 being the most abundant ones. We show that the AngII-induced Ca2+ entry but also Ca2+ release from intracellular stores are critically dependent on the density of CFs in culture and are inversely correlated with the expression of the myofibroblast marker α-smooth muscle actin. Our Ca2+ measurements depict that the AngII- and thrombin-induced Ca2+ transients, and the AngII-induced Ca2+ entry and Ca2+ release are not affected in CFs isolated from mice lacking all seven TRPC proteins (TRPC-hepta KO) compared to control cells. However, pre-incubation with GSK7975A (10 µM), which sufficiently inhibits CRAC channels in other cells, abolished AngII-induced Ca2+ entry. Consequently, we conclude the dispensability of the TRPC channels for the acute neurohumoral Ca2+ signaling evoked by AngII in isolated CFs and suggest the contribution of members of the Orai channel family as molecular constituents responsible for this pathophysiologically important Ca2+ entry pathway.
Fil: Camacho Londoño, Juan E.. Ruprecht Karls Universitat Heidelberg; Alemania
Fil: Marx, André. Ruprecht Karls Universitat Heidelberg; Alemania
Fil: Kraft, Axel E.. Ruprecht Karls Universitat Heidelberg; Alemania
Fil: Schürger, Alexander. Ruprecht Karls Universitat Heidelberg; Alemania
Fil: Richter, Christin. Ruprecht Karls Universitat Heidelberg; Alemania
Fil: Dietrich, Alexander. Ludwig Maximilians Universitat; Alemania
Fil: Lipp, Peter. Universitat Saarland; Alemania
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: Freichel, Marc. Ruprecht Karls Universitat Heidelberg; Alemania
description TRPC proteins form cation conducting channels regulated by different stimuli and are regulators of the cellular calcium homeostasis. TRPC are expressed in cardiac cells including cardiac fibroblasts (CFs) and have been implicated in the development of pathological cardiac remodeling including fibrosis. Using Ca2+ imaging and several compound TRPC knockout mouse lines we analyzed the involvement of TRPC proteins for the angiotensin II (AngII)-induced changes in Ca2+ homeostasis in CFs isolated from adult mice. Using qPCR we detected transcripts of all Trpc genes in CFs; Trpc1, Trpc3 and Trpc4 being the most abundant ones. We show that the AngII-induced Ca2+ entry but also Ca2+ release from intracellular stores are critically dependent on the density of CFs in culture and are inversely correlated with the expression of the myofibroblast marker α-smooth muscle actin. Our Ca2+ measurements depict that the AngII- and thrombin-induced Ca2+ transients, and the AngII-induced Ca2+ entry and Ca2+ release are not affected in CFs isolated from mice lacking all seven TRPC proteins (TRPC-hepta KO) compared to control cells. However, pre-incubation with GSK7975A (10 µM), which sufficiently inhibits CRAC channels in other cells, abolished AngII-induced Ca2+ entry. Consequently, we conclude the dispensability of the TRPC channels for the acute neurohumoral Ca2+ signaling evoked by AngII in isolated CFs and suggest the contribution of members of the Orai channel family as molecular constituents responsible for this pathophysiologically important Ca2+ entry pathway.
publishDate 2020
dc.date.none.fl_str_mv 2020-01
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/11336/141717
Camacho Londoño, Juan E.; Marx, André; Kraft, Axel E.; Schürger, Alexander; Richter, Christin; et al.; Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels; Molecular Diversity Preservation International; Cells; 9; 2; 1-2020; 1-27
2073-4409
2073-4409
CONICET Digital
CONICET
url http://hdl.handle.net/11336/141717
identifier_str_mv Camacho Londoño, Juan E.; Marx, André; Kraft, Axel E.; Schürger, Alexander; Richter, Christin; et al.; Angiotensin-II-Evoked Ca2+ Entry in Murine Cardiac Fibroblasts Does Not Depend on TRPC Channels; Molecular Diversity Preservation International; Cells; 9; 2; 1-2020; 1-27
2073-4409
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.3390/cells9020322
info:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/2073-4409/9/2/322
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 Molecular Diversity Preservation International
publisher.none.fl_str_mv Molecular Diversity Preservation International
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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score 13.13397

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