Murine cardiac growth, TRPC channels, and cGMP kinase I

Autores
Domes, Katrin; Patrucco, Enrico; Loga, Florian; Dietrich, Alexander; Birnbaumer, Lutz; Wegener, Jörg W.; Hofmann, Franz
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Signaling via cGMP-dependent protein kinase I (cGKI) and canonical transient receptor potential (TRPC) channels appears to be involved in the regulation of cardiac hypertrophy. Recent evidence suggests that TRPC channels are targets for cGKI, and phosphorylation of these channels may mediate the antihypertrophic effects of cGMP signaling. We tested this concept by investigating the role of cGMP/cGKI signaling on angiotensin II (A II)-induced cardiac hypertrophy using a control group (Ctr), trpc6−/−, trpc3−/−, trpc3−/−/6−/−, βRM mice, and trpc3−/−/6−/− × βRM mice. βRM mice express cGKIβ only in the smooth muscle on a cGKI−/− background. The control group was composed of littermate mice that contained at least one wild type gene of the respective genotype. A II was infused by minipumps (7 days; 2 mg/kg/day) in Ctr, trpc6−/−, trpc3−/−, trpc3−/−/6−/−, βRM, and trpc3−/−/6−/− × βRM mice. Hypertrophy was assessed by measuring heart weight per tibia length (HW/TL) and fibrosis by staining of heart slices. A II-induced increase in HW/TL and fibrosis was absent in trpc3−/− mice, whereas an increase in HW/TL and fibrosis was evident in Ctr and trpc6−/−, minimal or absent in trpc3−/−, moderate in βRM, and dramatic in trpc3−/−/6−/− βRM mice. These results suggest that TRPC3 may be necessary for A II-induced cardiac hypertrophy. On the other hand, hypertrophy and fibrosis were massively increased in βRM mice on a TRPC3/6 × cGKI−/−KO background, indicating an “additive” coupling between both signaling pathways.
Fil: Domes, Katrin. Universitat Technical Zu Munich; Alemania
Fil: Patrucco, Enrico. Universitat Technical Zu Munich; Alemania
Fil: Loga, Florian. Universitat Technical Zu Munich; Alemania
Fil: Dietrich, Alexander. Ludwig Maximilians Universitat; Alemania
Fil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institute of Environmental Health Sciences; Estados Unidos
Fil: Wegener, Jörg W.. Universitat Technical Zu Munich; Alemania
Fil: Hofmann, Franz. Universitat Technical Zu Munich; Alemania
Materia
CARDIAC MYOCYTES
ENDOTHELIUM/FIBROCYTES
NITRIC OXIDE/PKG-I
SIGNAL TRANSDUCTION
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:11336/95534
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/95534
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Murine cardiac growth, TRPC channels, and cGMP kinase IDomes, KatrinPatrucco, EnricoLoga, FlorianDietrich, AlexanderBirnbaumer, LutzWegener, Jörg W.Hofmann, FranzCARDIAC MYOCYTESENDOTHELIUM/FIBROCYTESNITRIC OXIDE/PKG-ISIGNAL TRANSDUCTIONTRPC CHANNELShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Signaling via cGMP-dependent protein kinase I (cGKI) and canonical transient receptor potential (TRPC) channels appears to be involved in the regulation of cardiac hypertrophy. Recent evidence suggests that TRPC channels are targets for cGKI, and phosphorylation of these channels may mediate the antihypertrophic effects of cGMP signaling. We tested this concept by investigating the role of cGMP/cGKI signaling on angiotensin II (A II)-induced cardiac hypertrophy using a control group (Ctr), trpc6−/−, trpc3−/−, trpc3−/−/6−/−, βRM mice, and trpc3−/−/6−/− × βRM mice. βRM mice express cGKIβ only in the smooth muscle on a cGKI−/− background. The control group was composed of littermate mice that contained at least one wild type gene of the respective genotype. A II was infused by minipumps (7 days; 2 mg/kg/day) in Ctr, trpc6−/−, trpc3−/−, trpc3−/−/6−/−, βRM, and trpc3−/−/6−/− × βRM mice. Hypertrophy was assessed by measuring heart weight per tibia length (HW/TL) and fibrosis by staining of heart slices. A II-induced increase in HW/TL and fibrosis was absent in trpc3−/− mice, whereas an increase in HW/TL and fibrosis was evident in Ctr and trpc6−/−, minimal or absent in trpc3−/−, moderate in βRM, and dramatic in trpc3−/−/6−/− βRM mice. These results suggest that TRPC3 may be necessary for A II-induced cardiac hypertrophy. On the other hand, hypertrophy and fibrosis were massively increased in βRM mice on a TRPC3/6 × cGKI−/−KO background, indicating an “additive” coupling between both signaling pathways.Fil: Domes, Katrin. Universitat Technical Zu Munich; AlemaniaFil: Patrucco, Enrico. Universitat Technical Zu Munich; AlemaniaFil: Loga, Florian. Universitat Technical Zu Munich; AlemaniaFil: Dietrich, Alexander. Ludwig Maximilians Universitat; AlemaniaFil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institute of Environmental Health Sciences; Estados UnidosFil: Wegener, Jörg W.. Universitat Technical Zu Munich; AlemaniaFil: Hofmann, Franz. Universitat Technical Zu Munich; AlemaniaSpringer2015-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/95534Domes, Katrin; Patrucco, Enrico; Loga, Florian; Dietrich, Alexander; Birnbaumer, Lutz; et al.; Murine cardiac growth, TRPC channels, and cGMP kinase I; Springer; Pflugers Archiv-European Journal of Physiology; 467; 10; 10-2015; 2229-22340031-6768CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007/s00424-014-1682-0info:eu-repo/semantics/altIdentifier/doi/10.1007/s00424-014-1682-0info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:44:33Zoai:ri.conicet.gov.ar:11336/95534instacron: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 09:44:33.65CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Murine cardiac growth, TRPC channels, and cGMP kinase I
title Murine cardiac growth, TRPC channels, and cGMP kinase I
spellingShingle Murine cardiac growth, TRPC channels, and cGMP kinase I
Domes, Katrin
CARDIAC MYOCYTES
ENDOTHELIUM/FIBROCYTES
NITRIC OXIDE/PKG-I
SIGNAL TRANSDUCTION
TRPC CHANNELS
title_short Murine cardiac growth, TRPC channels, and cGMP kinase I
title_full Murine cardiac growth, TRPC channels, and cGMP kinase I
title_fullStr Murine cardiac growth, TRPC channels, and cGMP kinase I
title_full_unstemmed Murine cardiac growth, TRPC channels, and cGMP kinase I
title_sort Murine cardiac growth, TRPC channels, and cGMP kinase I
dc.creator.none.fl_str_mv Domes, Katrin
Patrucco, Enrico
Loga, Florian
Dietrich, Alexander
Birnbaumer, Lutz
Wegener, Jörg W.
Hofmann, Franz
author Domes, Katrin
author_facet Domes, Katrin
Patrucco, Enrico
Loga, Florian
Dietrich, Alexander
Birnbaumer, Lutz
Wegener, Jörg W.
Hofmann, Franz
author_role author
author2 Patrucco, Enrico
Loga, Florian
Dietrich, Alexander
Birnbaumer, Lutz
Wegener, Jörg W.
Hofmann, Franz
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv CARDIAC MYOCYTES
ENDOTHELIUM/FIBROCYTES
NITRIC OXIDE/PKG-I
SIGNAL TRANSDUCTION
TRPC CHANNELS
topic CARDIAC MYOCYTES
ENDOTHELIUM/FIBROCYTES
NITRIC OXIDE/PKG-I
SIGNAL TRANSDUCTION
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 Signaling via cGMP-dependent protein kinase I (cGKI) and canonical transient receptor potential (TRPC) channels appears to be involved in the regulation of cardiac hypertrophy. Recent evidence suggests that TRPC channels are targets for cGKI, and phosphorylation of these channels may mediate the antihypertrophic effects of cGMP signaling. We tested this concept by investigating the role of cGMP/cGKI signaling on angiotensin II (A II)-induced cardiac hypertrophy using a control group (Ctr), trpc6−/−, trpc3−/−, trpc3−/−/6−/−, βRM mice, and trpc3−/−/6−/− × βRM mice. βRM mice express cGKIβ only in the smooth muscle on a cGKI−/− background. The control group was composed of littermate mice that contained at least one wild type gene of the respective genotype. A II was infused by minipumps (7 days; 2 mg/kg/day) in Ctr, trpc6−/−, trpc3−/−, trpc3−/−/6−/−, βRM, and trpc3−/−/6−/− × βRM mice. Hypertrophy was assessed by measuring heart weight per tibia length (HW/TL) and fibrosis by staining of heart slices. A II-induced increase in HW/TL and fibrosis was absent in trpc3−/− mice, whereas an increase in HW/TL and fibrosis was evident in Ctr and trpc6−/−, minimal or absent in trpc3−/−, moderate in βRM, and dramatic in trpc3−/−/6−/− βRM mice. These results suggest that TRPC3 may be necessary for A II-induced cardiac hypertrophy. On the other hand, hypertrophy and fibrosis were massively increased in βRM mice on a TRPC3/6 × cGKI−/−KO background, indicating an “additive” coupling between both signaling pathways.
Fil: Domes, Katrin. Universitat Technical Zu Munich; Alemania
Fil: Patrucco, Enrico. Universitat Technical Zu Munich; Alemania
Fil: Loga, Florian. Universitat Technical Zu Munich; Alemania
Fil: Dietrich, Alexander. Ludwig Maximilians Universitat; Alemania
Fil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institute of Environmental Health Sciences; Estados Unidos
Fil: Wegener, Jörg W.. Universitat Technical Zu Munich; Alemania
Fil: Hofmann, Franz. Universitat Technical Zu Munich; Alemania
description Signaling via cGMP-dependent protein kinase I (cGKI) and canonical transient receptor potential (TRPC) channels appears to be involved in the regulation of cardiac hypertrophy. Recent evidence suggests that TRPC channels are targets for cGKI, and phosphorylation of these channels may mediate the antihypertrophic effects of cGMP signaling. We tested this concept by investigating the role of cGMP/cGKI signaling on angiotensin II (A II)-induced cardiac hypertrophy using a control group (Ctr), trpc6−/−, trpc3−/−, trpc3−/−/6−/−, βRM mice, and trpc3−/−/6−/− × βRM mice. βRM mice express cGKIβ only in the smooth muscle on a cGKI−/− background. The control group was composed of littermate mice that contained at least one wild type gene of the respective genotype. A II was infused by minipumps (7 days; 2 mg/kg/day) in Ctr, trpc6−/−, trpc3−/−, trpc3−/−/6−/−, βRM, and trpc3−/−/6−/− × βRM mice. Hypertrophy was assessed by measuring heart weight per tibia length (HW/TL) and fibrosis by staining of heart slices. A II-induced increase in HW/TL and fibrosis was absent in trpc3−/− mice, whereas an increase in HW/TL and fibrosis was evident in Ctr and trpc6−/−, minimal or absent in trpc3−/−, moderate in βRM, and dramatic in trpc3−/−/6−/− βRM mice. These results suggest that TRPC3 may be necessary for A II-induced cardiac hypertrophy. On the other hand, hypertrophy and fibrosis were massively increased in βRM mice on a TRPC3/6 × cGKI−/−KO background, indicating an “additive” coupling between both signaling pathways.
publishDate 2015
dc.date.none.fl_str_mv 2015-10
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/11336/95534
Domes, Katrin; Patrucco, Enrico; Loga, Florian; Dietrich, Alexander; Birnbaumer, Lutz; et al.; Murine cardiac growth, TRPC channels, and cGMP kinase I; Springer; Pflugers Archiv-European Journal of Physiology; 467; 10; 10-2015; 2229-2234
0031-6768
CONICET Digital
CONICET
url http://hdl.handle.net/11336/95534
identifier_str_mv Domes, Katrin; Patrucco, Enrico; Loga, Florian; Dietrich, Alexander; Birnbaumer, Lutz; et al.; Murine cardiac growth, TRPC channels, and cGMP kinase I; Springer; Pflugers Archiv-European Journal of Physiology; 467; 10; 10-2015; 2229-2234
0031-6768
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007/s00424-014-1682-0
info:eu-repo/semantics/altIdentifier/doi/10.1007/s00424-014-1682-0
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
application/pdf
dc.publisher.none.fl_str_mv Springer
publisher.none.fl_str_mv Springer
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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