Angiotensin-II-evoked Ca2+ entry in murine cardiac gibroblasts 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
español castellano
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Fil: Camacho Londoño, Juan E. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; Alemania
Fil: Camacho Londoño, Juan E. German Centre for Cardiovascular Research; Alemania
Fil: Marx, André. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; Alemania
Fil: Kraft, Axel E. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; Alemania
Fil: Kraft, Axel E. German Centre for Cardiovascular Research; Alemania
Fil: Schürger, Alexander. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; Alemania
Fil: Schürger, Alexander. German Centre for Cardiovascular Research; Alemania
Fil: Richter, Christin. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; Alemania
Fil: Dietrich, Alexander. Ludwig-Maximilians-Universität. Walther-Straub-Institut für Pharmakologie und Toxikologie; Alemania
Fil: Lipp, Peter. Saarland University; Alemania
Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados Unidos
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentina
Fil: Freichel, Marc. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; Alemania
Fil: Freichel, Marc. German Centre for Cardiovascular Research; Alemania
Abstract: 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.
Fuente
Cells. 2020, 9(2)
Materia
CALCIO
MIOCARDIO
GENES
TRPC
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
Repositorio Institucional (UCA)
Institución
Pontificia Universidad Católica Argentina
OAI Identificador
oai:ucacris:123456789/14246

id RIUCA_223e2d19d47442e9436a92da6854d139
oai_identifier_str oai:ucacris:123456789/14246
network_acronym_str RIUCA
repository_id_str 2585
network_name_str Repositorio Institucional (UCA)
spelling Angiotensin-II-evoked Ca2+ entry in murine cardiac gibroblasts does not depend on TRPC channelsCamacho Londoño, Juan E.Marx, AndréKraft, Axel E.Schürger, AlexanderRichter, ChristinDietrich, AlexanderLipp, PeterBirnbaumer, LutzFreichel, MarcCALCIOMIOCARDIOGENESTRPCFil: Camacho Londoño, Juan E. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; AlemaniaFil: Camacho Londoño, Juan E. German Centre for Cardiovascular Research; AlemaniaFil: Marx, André. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; AlemaniaFil: Kraft, Axel E. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; AlemaniaFil: Kraft, Axel E. German Centre for Cardiovascular Research; AlemaniaFil: Schürger, Alexander. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; AlemaniaFil: Schürger, Alexander. German Centre for Cardiovascular Research; AlemaniaFil: Richter, Christin. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; AlemaniaFil: Dietrich, Alexander. Ludwig-Maximilians-Universität. Walther-Straub-Institut für Pharmakologie und Toxikologie; AlemaniaFil: Lipp, Peter. Saarland University; AlemaniaFil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados UnidosFil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; ArgentinaFil: Freichel, Marc. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; AlemaniaFil: Freichel, Marc. German Centre for Cardiovascular Research; AlemaniaAbstract: 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.MDPI2020info: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/123456789/142462073-440910.3390/cells902032232013125Camacho Londoño, J.E., et al. Angiotensin-II-evoked Ca2+ entry in murine cardiac gibroblasts does not depend on TRPC channels [en línea]. Cells. 2020, 9(2) doi:10.3390/cells9020322 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14246Cells. 2020, 9(2)reponame:Repositorio Institucional (UCA)instname:Pontificia Universidad Católica Argentinaspainfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/4.0/2025-07-03T10:58:38Zoai:ucacris:123456789/14246instacron:UCAInstitucionalhttps://repositorio.uca.edu.ar/Universidad privadaNo correspondehttps://repositorio.uca.edu.ar/oaiclaudia_fernandez@uca.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:25852025-07-03 10:58:38.39Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentinafalse
dc.title.none.fl_str_mv Angiotensin-II-evoked Ca2+ entry in murine cardiac gibroblasts does not depend on TRPC channels
title Angiotensin-II-evoked Ca2+ entry in murine cardiac gibroblasts does not depend on TRPC channels
spellingShingle Angiotensin-II-evoked Ca2+ entry in murine cardiac gibroblasts does not depend on TRPC channels
Camacho Londoño, Juan E.
CALCIO
MIOCARDIO
GENES
TRPC
title_short Angiotensin-II-evoked Ca2+ entry in murine cardiac gibroblasts does not depend on TRPC channels
title_full Angiotensin-II-evoked Ca2+ entry in murine cardiac gibroblasts does not depend on TRPC channels
title_fullStr Angiotensin-II-evoked Ca2+ entry in murine cardiac gibroblasts does not depend on TRPC channels
title_full_unstemmed Angiotensin-II-evoked Ca2+ entry in murine cardiac gibroblasts does not depend on TRPC channels
title_sort Angiotensin-II-evoked Ca2+ entry in murine cardiac gibroblasts 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 CALCIO
MIOCARDIO
GENES
TRPC
topic CALCIO
MIOCARDIO
GENES
TRPC
dc.description.none.fl_txt_mv Fil: Camacho Londoño, Juan E. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; Alemania
Fil: Camacho Londoño, Juan E. German Centre for Cardiovascular Research; Alemania
Fil: Marx, André. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; Alemania
Fil: Kraft, Axel E. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; Alemania
Fil: Kraft, Axel E. German Centre for Cardiovascular Research; Alemania
Fil: Schürger, Alexander. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; Alemania
Fil: Schürger, Alexander. German Centre for Cardiovascular Research; Alemania
Fil: Richter, Christin. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; Alemania
Fil: Dietrich, Alexander. Ludwig-Maximilians-Universität. Walther-Straub-Institut für Pharmakologie und Toxikologie; Alemania
Fil: Lipp, Peter. Saarland University; Alemania
Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados Unidos
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentina
Fil: Freichel, Marc. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; Alemania
Fil: Freichel, Marc. German Centre for Cardiovascular Research; Alemania
Abstract: 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.
description Fil: Camacho Londoño, Juan E. Ruprecht-Karls-Universität Heidelberg. Pharmakologisches Institut; Alemania
publishDate 2020
dc.date.none.fl_str_mv 2020
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/123456789/14246
2073-4409
10.3390/cells9020322
32013125
Camacho Londoño, J.E., et al. Angiotensin-II-evoked Ca2+ entry in murine cardiac gibroblasts does not depend on TRPC channels [en línea]. Cells. 2020, 9(2) doi:10.3390/cells9020322 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14246
url https://repositorio.uca.edu.ar/handle/123456789/14246
identifier_str_mv 2073-4409
10.3390/cells9020322
32013125
Camacho Londoño, J.E., et al. Angiotensin-II-evoked Ca2+ entry in murine cardiac gibroblasts does not depend on TRPC channels [en línea]. Cells. 2020, 9(2) doi:10.3390/cells9020322 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14246
dc.language.none.fl_str_mv spa
language spa
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 MDPI
publisher.none.fl_str_mv MDPI
dc.source.none.fl_str_mv Cells. 2020, 9(2)
reponame:Repositorio Institucional (UCA)
instname:Pontificia Universidad Católica Argentina
reponame_str Repositorio Institucional (UCA)
collection Repositorio Institucional (UCA)
instname_str 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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score 13.13397