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dc.contributor.author
Han, Jung Woo
dc.contributor.author
Lee, Young Ho
dc.contributor.author
Yoen, Su-In
dc.contributor.author
Abramowitz, Joel
dc.contributor.author
Birnbaumer, Lutz
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dc.contributor.author
Lee, Min Goo
dc.contributor.author
Kim, Joo Young
dc.date.available
2018-03-22T15:41:25Z
dc.date.issued
2016-10
dc.identifier.citation
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
dc.identifier.issn
0300-8177
dc.identifier.uri
http://hdl.handle.net/11336/39653
dc.description.abstract
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.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Springer
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Ca2+ Influx
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L-Type Ca2+ Channel
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Pathologic Cardiac Hypertrophy
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Transient Receptor Potential Canonical Channels 3
dc.subject.classification
Inmunología
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dc.subject.classification
Medicina Básica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-03-20T14:33:42Z
dc.identifier.eissn
1573-4919
dc.journal.volume
421
dc.journal.number
1-2
dc.journal.pagination
55-65
dc.journal.pais
Alemania
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dc.description.fil
Fil: Han, Jung Woo. Yonsei University College of Medicine; Corea del Sur
dc.description.fil
Fil: Lee, Young Ho. Yonsei University College of Medicine; Corea del Sur
dc.description.fil
Fil: Yoen, Su-In. Yonsei University College of Medicine; Corea del Sur
dc.description.fil
Fil: Abramowitz, Joel. National Institute of Environmental Health Sciences; Estados Unidos
dc.description.fil
Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.description.fil
Fil: Lee, Min Goo. Yonsei University College of Medicine; Corea del Sur
dc.description.fil
Fil: Kim, Joo Young. Yonsei University College of Medicine; Corea del Sur
dc.journal.title
Molecular and Cellular Biochemistry
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s11010-016-2784-0
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11010-016-2784-0
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