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dc.contributor.author
Oda, Sayaka
dc.contributor.author
Numaga Tomita, Takuro
dc.contributor.author
Kitajima, Naoyuki
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Tomizaki, Takashi
dc.contributor.author
Harada, Eri
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Shimauchi, Tsukasa
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Nishimura, Akiyuki
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Ishikawa, Tatsuya
dc.contributor.author
Kumagai, Yoshito
dc.contributor.author
Birnbaumer, Lutz
dc.contributor.author
Nishida, Motohiro
dc.date.available
2018-06-15T17:30:13Z
dc.date.issued
2017-08
dc.identifier.citation
Oda, Sayaka; Numaga Tomita, Takuro; Kitajima, Naoyuki; Tomizaki, Takashi; Harada, Eri; et al.; TRPC6 counteracts TRPC3-Nox2 protein complex leading to attenuation of hyperglycemia-induced heart failure in mice; Sci Rep; Scientific Reports; 7; 1; 8-2017; 1-14
dc.identifier.issn
2045-2322
dc.identifier.uri
http://hdl.handle.net/11336/48809
dc.description.abstract
Excess production of reactive oxygen species (ROS) caused by hyperglycemia is a major risk factor for heart failure. We previously reported that transient receptor potential canonical 3 (TRPC3) channel mediates pressure overload-induced maladaptive cardiac fibrosis by forming stably functional complex with NADPH oxidase 2 (Nox2). Although TRPC3 has been long suggested to form hetero-multimer channels with TRPC6 and function as diacylglycerol-activated cation channels coordinately, the role of TRPC6 in heart is still obscure. We here demonstrated that deletion of TRPC6 had no impact on pressure overload-induced heart failure despite inhibiting interstitial fibrosis in mice. TRPC6-deficient mouse hearts 1 week after transverse aortic constriction showed comparable increases in fibrotic gene expressions and ROS production but promoted inductions of inflammatory cytokines, compared to wild type hearts. Treatment of TRPC6-deficient mice with streptozotocin caused severe reduction of cardiac contractility with enhancing urinary and cardiac lipid peroxide levels, compared to wild type and TRPC3-deficient mice. Knockdown of TRPC6, but not TRPC3, enhanced basal expression levels of cytokines in rat cardiomyocytes. TRPC6 could interact with Nox2, but the abundance of TRPC6 was inversely correlated with that of Nox2. These results strongly suggest that Nox2 destabilization through disrupting TRPC3-Nox2 complex underlies attenuation of hyperglycemia-induced heart failure by TRPC6.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Sci Rep
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Trpc6 Counteracts Trpc3-Nox2 Protein Complex Leading to Attenuation Of Hyperglycemia-Induced Heart Failure In Mice
dc.subject
Trpc3-Nox2
dc.subject
Trpc6
dc.subject
Hyperglycemia
dc.subject.classification
Otras Ciencias Biológicas
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Ciencias Biológicas
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CIENCIAS NATURALES Y EXACTAS
dc.title
TRPC6 counteracts TRPC3-Nox2 protein complex leading to attenuation of hyperglycemia-induced heart failure in 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
2018-06-07T14:27:49Z
dc.journal.volume
7
dc.journal.number
1
dc.journal.pagination
1-14
dc.journal.pais
Reino Unido
dc.journal.ciudad
Londres
dc.description.fil
Fil: Oda, Sayaka. Okazaki Institute for Integrative Bioscience; Japón. SOKENDAI; Japón
dc.description.fil
Fil: Numaga Tomita, Takuro. Okazaki Institute for Integrative Bioscience; Japón. SOKENDAI; Japón
dc.description.fil
Fil: Kitajima, Naoyuki. Okazaki Institute for Integrative Bioscience; Japón. Kyushu University; Japón
dc.description.fil
Fil: Tomizaki, Takashi. Okazaki Institute for Integrative Bioscience; Japón. Kyushu University; Japón. University of Tsukuba; Japón
dc.description.fil
Fil: Harada, Eri. Ajinomoto Co.; Japón. EA Pharma Co.; Japón
dc.description.fil
Fil: Shimauchi, Tsukasa. Okazaki Institute for Integrative Bioscience; Japón. Kyushu University; Japón
dc.description.fil
Fil: Nishimura, Akiyuki. Okazaki Institute for Integrative Bioscience; Japón. SOKENDAI; Japón. Ajinomoto Co.; Japón
dc.description.fil
Fil: Ishikawa, Tatsuya. Kyushu University; Japón. Ajinomoto Co.; Japón. EA Pharma Co.; Japón
dc.description.fil
Fil: Kumagai, Yoshito. University of Tsukuba; Japón
dc.description.fil
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
dc.description.fil
Fil: Nishida, Motohiro. Okazaki Institute for Integrative Bioscience; Japón. SOKENDAI; Japón. Kyushu University; Japón. PRESTO; Japón
dc.journal.title
Scientific Reports
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/s41598-017-07903-4
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1038/s41598-017-07903-4
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