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Campo DC | Valor | Lengua/Idioma |
---|---|---|
dc.contributor.author | Numaga-Tomita, Takuro | es |
dc.contributor.author | Kitajima, Naoyuki | es |
dc.contributor.author | Kuroda, Takuya | es |
dc.contributor.author | Nishimura, Akiyuki | es |
dc.contributor.author | Miyano, Kei | es |
dc.contributor.author | Yasuda, Satoshi | es |
dc.contributor.author | Kuwahara, Koichiro | es |
dc.contributor.author | Sato, Yoji | es |
dc.contributor.author | Ide, Tomomi | es |
dc.contributor.author | Birnbaumer, Lutz | es |
dc.contributor.author | Sumimoto, Hideki | es |
dc.contributor.author | Mori, Yasuo | es |
dc.contributor.author | Nishida, Motohiro | es |
dc.date.accessioned | 2019-09-16T20:15:04Z | - |
dc.date.available | 2019-09-16T20:15:04Z | - |
dc.date.issued | 2016 | - |
dc.identifier.citation | Numaga-Tomita T, Kitajima N, Kuroda T, et al. TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis [en línea]. Scientific Reports. 2016;6:39383. doi:10.1038/srep39383 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8746 | es |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | https://repositorio.uca.edu.ar/handle/123456789/8746 | - |
dc.description.abstract | Abstract: Structural cardiac remodeling, accompanying cytoskeletal reorganization of cardiac cells, is a major clinical outcome of diastolic heart failure. A highly local Ca2+ influx across the plasma membrane has been suggested to code signals to induce Rho GTPase-mediated fibrosis, but it is obscure how the heart specifically decodes the local Ca2+ influx as a cytoskeletal reorganizing signal under the conditions of the rhythmic Ca2+ handling required for pump function. We found that an inhibition of transient receptor potential canonical 3 (TRPC3) channel activity exhibited resistance to Rho-mediated maladaptive fibrosis in pressure-overloaded mouse hearts. Proteomic analysis revealed that microtubule-associated Rho guanine nucleotide exchange factor, GEF-H1, participates in TRPC3-mediated RhoA activation induced by mechanical stress in cardiomyocytes and transforming growth factor (TGF) β stimulation in cardiac fibroblasts. We previously revealed that TRPC3 functionally interacts with microtubule-associated NADPH oxidase (Nox) 2, and inhibition of Nox2 attenuated mechanical stretch-induced GEF-H1 activation in cardiomyocytes. Finally, pharmacological TRPC3 inhibition significantly suppressed fibrotic responses in human cardiomyocytes and cardiac fibroblasts. These results strongly suggest that microtubule-localized TRPC3-GEF-H1 axis mediates fibrotic responses commonly in cardiac myocytes and fibroblasts induced by physico-chemical stimulation. | es |
dc.format | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | Nature Research | es |
dc.rights | Acceso Abierto | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | * |
dc.source | Scientific Reports. 2016;6:39383 | es |
dc.subject | FIBROSIS | es |
dc.subject | CORAZON | es |
dc.subject | CRECIMIENTO | es |
dc.subject | CELULAS | es |
dc.title | TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis | es |
dc.type | Artículo | es |
dc.identifier.doi | 10.1038/srep39383 | - |
dc.identifier.pmid | 27991560 | - |
uca.disciplina | MEDICINA | es |
uca.issnrd | 1 | es |
uca.affiliation | Fil: Numaga-Tomita, Takuro. National Institute for Physiological Sciences. Okazaki Institute for Integrative Bioscience. Division of Cardiocirculatory Signaling; Japón | es |
uca.affiliation | Fil: Numaga-Tomita, Takuro. The Graduate University for Advanced Studies. School of Life Science. Department of Physiological Sciences; Japón | es |
uca.affiliation | Fil: Kitajima, Naoyuki. National Institute for Physiological Sciences. Okazaki Institute for Integrative Bioscience. Division of Cardiocirculatory Signaling; Japón | es |
uca.affiliation | Fil: Kitajima, Naoyuki. Kyushu University. Graduate School of Pharmaceutical Sciences. Department of Translational Pharmaceutical Sciences; Japón | es |
uca.affiliation | Fil: Kuroda, Takuya. National Institute of Health Sciences. Division of Cell-Based Therapeutic Products; Japón | es |
uca.affiliation | Fil: Nishimura, Akiyuki. National Institute for Physiological Sciences. Okazaki Institute for Integrative Bioscience. Division of Cardiocirculatory Signaling; Japón | es |
uca.affiliation | Fil: Nishimura, Akiyuki. The Graduate University for Advanced Studies. School of Life Science. Department of Physiological Sciences; Japón | es |
uca.affiliation | Fil: Miyano, Kei. Kyushu University. Graduate School of Medical Sciences. Department of Biochemistry; Japón | es |
uca.affiliation | Fil: Yasuda, Satoshi. National Institute of Health Sciences. Division of Cell-Based Therapeutic Products; Japón | es |
uca.affiliation | Fil: Kuwahara, Koichiro. Shinshu University. School of Medicine. Department of Cardiovascular Medicine; Japón | es |
uca.affiliation | Fil: Sato, Yoji. Kyushu University. Graduate School of Pharmaceutical Sciences. Department of Translational Pharmaceutical Sciences; Japón | es |
uca.affiliation | Fil: Sato, Yoji. National Institute of Health Sciences. Division of Cell-Based Therapeutic Products; Japón | es |
uca.affiliation | Fil: Ide, Tomomi. Kyushu University. Graduate School of Medical Sciences. Department of Cardiovascular Medicine; Argentina | es |
uca.affiliation | Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentina | es |
uca.affiliation | Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados Unidos | es |
uca.affiliation | Fil: Sumimoto, Hideki. Kyushu University. Graduate School of Medical Sciences. Department of Biochemistry; Japón | es |
uca.affiliation | Fil: Mori, Yasuo. Kyoto University. Graduate School of Engineering. Department of Synthetic Chemistry and Biological Chemistry; Japón | es |
uca.affiliation | Fil: Nishida, Motohiro. National Institute for Physiological Sciences. Okazaki Institute for Integrative Bioscience. Division of Cardiocirculatory Signaling; Japón | es |
uca.affiliation | Fil: Nishida, Motohiro. The Graduate University for Advanced Studies. School of Life Science. Department of Physiological Sciences; Japón | es |
uca.affiliation | Fil: Nishida, Motohiro. Kyushu University. Graduate School of Pharmaceutical Sciences. Department of Translational Pharmaceutical Sciences; Japón | es |
uca.affiliation | Fil: Nishida, Motohiro. Precursory Research for Embryonic Science and Technology; Japón | es |
uca.version | publishedVersion | es |
item.fulltext | With Fulltext | - |
item.grantfulltext | open | - |
item.languageiso639-1 | en | - |
crisitem.author.dept | Instituto de Investigaciones Biomédicas - BIOMED | - |
crisitem.author.dept | Laboratorio de Función y Farmacología de Canales Iónicos | - |
crisitem.author.dept | Consejo Nacional de Investigaciones Científicas y Técnicas | - |
crisitem.author.dept | Facultad de Ciencias Médicas | - |
crisitem.author.orcid | 0000-0002-0775-8661 | - |
crisitem.author.parentorg | Facultad de Ciencias Médicas | - |
crisitem.author.parentorg | Instituto de Investigaciones Biomédicas - BIOMED | - |
crisitem.author.parentorg | Pontificia Universidad Católica Argentina | - |
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