Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice

Autores
Han, Jung Woo; Lee, Young Ho; Yoen, Su-In; Abramowitz, Joel; Birnbaumer, Lutz; Lee, Min Goo; Kim, Joo Young
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Sustained elevation of intracellular Ca2+ concentration ([Ca2+]i) reprograms cardiovascular cell fate, leading to cellular hypertrophy via Ca2+-calmodulin/calcineurin (Cn)/NFAT activation. Accumulating evidence suggests that transient receptor potential canonical (Trpc) channels play important roles in the development of pathologic cardiac hypertrophy. Here, we demonstrated that Trpc3 mediates pathologic cardiac hypertrophy in neurohumoral elevation via direct regulation of CaV1.2 expressions. Elevated PE (phenylephrine) was maintained in mice by continuous infusion using an osmotic pump. Wild-type (WT) mice, but not Trpc3−/− showed a sudden decrease in blood pressure (BP) or death following elevation of BP under conditions of elevated PE. Trpc3−/− mesenteric artery showed decreased PE-stimulated vasoconstriction. Analysis of morphology, function, and pathologic marker expression revealed that PE elevation caused pathologic cardiac hypertrophy in WT mice, which was prevented by deletion of Trpc3. Interestingly, protection by Trpc3 deletion seemed to be a result of reduced cardiac CaV1.2 expressions. Basal and PE induced increased expression of protein and mRNA of CaV1.2 was decreased in Trpc3−/− heart. Accordingly, altered expression of CaV1.2 was observed by knockdown or stimulation of Trpc3 in cardiomyocytes. These findings suggest that Trpc3 is a mediator of pathologic cardiac hypertrophy not only through mediating part of the Ca2+ influx, but also through control of CaV1.2 expressions.
Fil: Han, Jung Woo. Yonsei University College of Medicine; Corea del Sur
Fil: Lee, Young Ho. Yonsei University College of Medicine; Corea del Sur
Fil: Yoen, Su-In. Yonsei University College of Medicine; Corea del Sur
Fil: Abramowitz, Joel. National Institute of Environmental Health Sciences; Estados Unidos
Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Lee, Min Goo. Yonsei University College of Medicine; Corea del Sur
Fil: Kim, Joo Young. Yonsei University College of Medicine; Corea del Sur
Materia
Ca2+ Influx
L-Type Ca2+ Channel
Pathologic Cardiac Hypertrophy
Transient Receptor Potential Canonical Channels 3
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:11336/39653
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/39653
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted miceHan, Jung WooLee, Young HoYoen, Su-InAbramowitz, JoelBirnbaumer, LutzLee, Min GooKim, Joo YoungCa2+ InfluxL-Type Ca2+ ChannelPathologic Cardiac HypertrophyTransient Receptor Potential Canonical Channels 3https://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Sustained elevation of intracellular Ca2+ concentration ([Ca2+]i) reprograms cardiovascular cell fate, leading to cellular hypertrophy via Ca2+-calmodulin/calcineurin (Cn)/NFAT activation. Accumulating evidence suggests that transient receptor potential canonical (Trpc) channels play important roles in the development of pathologic cardiac hypertrophy. Here, we demonstrated that Trpc3 mediates pathologic cardiac hypertrophy in neurohumoral elevation via direct regulation of CaV1.2 expressions. Elevated PE (phenylephrine) was maintained in mice by continuous infusion using an osmotic pump. Wild-type (WT) mice, but not Trpc3−/− showed a sudden decrease in blood pressure (BP) or death following elevation of BP under conditions of elevated PE. Trpc3−/− mesenteric artery showed decreased PE-stimulated vasoconstriction. Analysis of morphology, function, and pathologic marker expression revealed that PE elevation caused pathologic cardiac hypertrophy in WT mice, which was prevented by deletion of Trpc3. Interestingly, protection by Trpc3 deletion seemed to be a result of reduced cardiac CaV1.2 expressions. Basal and PE induced increased expression of protein and mRNA of CaV1.2 was decreased in Trpc3−/− heart. Accordingly, altered expression of CaV1.2 was observed by knockdown or stimulation of Trpc3 in cardiomyocytes. These findings suggest that Trpc3 is a mediator of pathologic cardiac hypertrophy not only through mediating part of the Ca2+ influx, but also through control of CaV1.2 expressions.Fil: Han, Jung Woo. Yonsei University College of Medicine; Corea del SurFil: Lee, Young Ho. Yonsei University College of Medicine; Corea del SurFil: Yoen, Su-In. Yonsei University College of Medicine; Corea del SurFil: Abramowitz, Joel. National Institute of Environmental Health Sciences; Estados UnidosFil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Lee, Min Goo. Yonsei University College of Medicine; Corea del SurFil: Kim, Joo Young. Yonsei University College of Medicine; Corea del SurSpringer2016-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/39653Han, Jung Woo; Lee, Young Ho; Yoen, Su-In; Abramowitz, Joel; Birnbaumer, Lutz; et al.; Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice; Springer; Molecular and Cellular Biochemistry; 421; 1-2; 10-2016; 55-650300-81771573-4919CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1007/s11010-016-2784-0info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11010-016-2784-0info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:52:45Zoai:ri.conicet.gov.ar:11336/39653instacron: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 09:52:45.435CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice
title Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice
spellingShingle Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice
Han, Jung Woo
Ca2+ Influx
L-Type Ca2+ Channel
Pathologic Cardiac Hypertrophy
Transient Receptor Potential Canonical Channels 3
title_short Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice
title_full Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice
title_fullStr Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice
title_full_unstemmed Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice
title_sort Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice
dc.creator.none.fl_str_mv Han, Jung Woo
Lee, Young Ho
Yoen, Su-In
Abramowitz, Joel
Birnbaumer, Lutz
Lee, Min Goo
Kim, Joo Young
author Han, Jung Woo
author_facet Han, Jung Woo
Lee, Young Ho
Yoen, Su-In
Abramowitz, Joel
Birnbaumer, Lutz
Lee, Min Goo
Kim, Joo Young
author_role author
author2 Lee, Young Ho
Yoen, Su-In
Abramowitz, Joel
Birnbaumer, Lutz
Lee, Min Goo
Kim, Joo Young
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Ca2+ Influx
L-Type Ca2+ Channel
Pathologic Cardiac Hypertrophy
Transient Receptor Potential Canonical Channels 3
topic Ca2+ Influx
L-Type Ca2+ Channel
Pathologic Cardiac Hypertrophy
Transient Receptor Potential Canonical Channels 3
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Sustained elevation of intracellular Ca2+ concentration ([Ca2+]i) reprograms cardiovascular cell fate, leading to cellular hypertrophy via Ca2+-calmodulin/calcineurin (Cn)/NFAT activation. Accumulating evidence suggests that transient receptor potential canonical (Trpc) channels play important roles in the development of pathologic cardiac hypertrophy. Here, we demonstrated that Trpc3 mediates pathologic cardiac hypertrophy in neurohumoral elevation via direct regulation of CaV1.2 expressions. Elevated PE (phenylephrine) was maintained in mice by continuous infusion using an osmotic pump. Wild-type (WT) mice, but not Trpc3−/− showed a sudden decrease in blood pressure (BP) or death following elevation of BP under conditions of elevated PE. Trpc3−/− mesenteric artery showed decreased PE-stimulated vasoconstriction. Analysis of morphology, function, and pathologic marker expression revealed that PE elevation caused pathologic cardiac hypertrophy in WT mice, which was prevented by deletion of Trpc3. Interestingly, protection by Trpc3 deletion seemed to be a result of reduced cardiac CaV1.2 expressions. Basal and PE induced increased expression of protein and mRNA of CaV1.2 was decreased in Trpc3−/− heart. Accordingly, altered expression of CaV1.2 was observed by knockdown or stimulation of Trpc3 in cardiomyocytes. These findings suggest that Trpc3 is a mediator of pathologic cardiac hypertrophy not only through mediating part of the Ca2+ influx, but also through control of CaV1.2 expressions.
Fil: Han, Jung Woo. Yonsei University College of Medicine; Corea del Sur
Fil: Lee, Young Ho. Yonsei University College of Medicine; Corea del Sur
Fil: Yoen, Su-In. Yonsei University College of Medicine; Corea del Sur
Fil: Abramowitz, Joel. National Institute of Environmental Health Sciences; Estados Unidos
Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Lee, Min Goo. Yonsei University College of Medicine; Corea del Sur
Fil: Kim, Joo Young. Yonsei University College of Medicine; Corea del Sur
description Sustained elevation of intracellular Ca2+ concentration ([Ca2+]i) reprograms cardiovascular cell fate, leading to cellular hypertrophy via Ca2+-calmodulin/calcineurin (Cn)/NFAT activation. Accumulating evidence suggests that transient receptor potential canonical (Trpc) channels play important roles in the development of pathologic cardiac hypertrophy. Here, we demonstrated that Trpc3 mediates pathologic cardiac hypertrophy in neurohumoral elevation via direct regulation of CaV1.2 expressions. Elevated PE (phenylephrine) was maintained in mice by continuous infusion using an osmotic pump. Wild-type (WT) mice, but not Trpc3−/− showed a sudden decrease in blood pressure (BP) or death following elevation of BP under conditions of elevated PE. Trpc3−/− mesenteric artery showed decreased PE-stimulated vasoconstriction. Analysis of morphology, function, and pathologic marker expression revealed that PE elevation caused pathologic cardiac hypertrophy in WT mice, which was prevented by deletion of Trpc3. Interestingly, protection by Trpc3 deletion seemed to be a result of reduced cardiac CaV1.2 expressions. Basal and PE induced increased expression of protein and mRNA of CaV1.2 was decreased in Trpc3−/− heart. Accordingly, altered expression of CaV1.2 was observed by knockdown or stimulation of Trpc3 in cardiomyocytes. These findings suggest that Trpc3 is a mediator of pathologic cardiac hypertrophy not only through mediating part of the Ca2+ influx, but also through control of CaV1.2 expressions.
publishDate 2016
dc.date.none.fl_str_mv 2016-10
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/11336/39653
Han, Jung Woo; Lee, Young Ho; Yoen, Su-In; Abramowitz, Joel; Birnbaumer, Lutz; et al.; Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice; Springer; Molecular and Cellular Biochemistry; 421; 1-2; 10-2016; 55-65
0300-8177
1573-4919
CONICET Digital
CONICET
url http://hdl.handle.net/11336/39653
identifier_str_mv Han, Jung Woo; Lee, Young Ho; Yoen, Su-In; Abramowitz, Joel; Birnbaumer, Lutz; et al.; Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice; Springer; Molecular and Cellular Biochemistry; 421; 1-2; 10-2016; 55-65
0300-8177
1573-4919
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1007/s11010-016-2784-0
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11010-016-2784-0
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
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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