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
- Institución
- Pontificia Universidad Católica Argentina
- OAI Identificador
- oai:ucacris:123456789/14246
Ver los metadatos del registro completo
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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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13.13397 |