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https://repositorio.uca.edu.ar/handle/123456789/8732
Campo DC | Valor | Lengua/Idioma |
---|---|---|
dc.contributor.author | Solanki, Sumeet | es |
dc.contributor.author | Dube, Prabhatchandra R. | es |
dc.contributor.author | Birnbaumer, Lutz | es |
dc.contributor.author | Vazquez, Guillermo | es |
dc.date.accessioned | 2019-09-12T19:22:29Z | - |
dc.date.available | 2019-09-12T19:22:29Z | - |
dc.date.issued | 2017 | - |
dc.identifier.citation | Solanki S, Dube PR, Birnbaumer L, Vazquez G. Reduced Necrosis and Content of Apoptotic M1 Macrophages in Advanced Atherosclerotic Plaques of Mice With Macrophage-Specific Loss of Trpc3 [en línea]. Scientific Reports. 2017;7:42526. doi:10.1038/srep42526 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8732 | es |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | https://repositorio.uca.edu.ar/handle/123456789/8732 | - |
dc.description.abstract | Abstract: In previous work we reported that ApoeKO mice transplanted with bone marrow cells deficient in the Transient Receptor Potential Canonical 3 (TRPC3) channel have reduced necrosis and number of apoptotic macrophages in advanced atherosclerotic plaques. Also, in vitro studies with polarized macrophages derived from mice with macrophage-specific loss of TRPC3 showed that M1, but not M2 macrophages, deficient in Trpc3 are less susceptible to ER stress-induced apoptosis than Trpc3 expressing cells. The questions remained (a) whether the plaque phenotype in transplanted mice resulted from a genuine effect of Trpc3 on macrophages, and (b) whether the reduced necrosis and macrophage apoptosis in plaques of these mice was a manifestation of the selective effect of TRPC3 on apoptosis of M1 macrophages previously observed in vitro. Here, we addressed these questions using Ldlr knockout (Ldlr-/-) mice with macrophage-specific loss of Trpc3 (MacTrpc3-/-/Ldlr-/- → Ldlr-/-). Compared to controls, we observed decreased plaque necrosis and number of apoptotic macrophages in MacTrpc3-/-/Ldlr-/- → Ldlr-/- mice. Immunohistochemical analysis revealed a reduction in apoptotic M1, but not apoptotic M2 macrophages. These findings confirm an effect of TRPC3 on plaque necrosis and support the notion that this is likely a reflection of the reduced susceptibility of Trpc3-deficient M1 macrophages to apoptosis. | 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. 2017;7:42526 | es |
dc.subject | NECROSIS | es |
dc.subject | APOPTOSIS | es |
dc.subject | ARTERIOESCLEROSIS | es |
dc.subject | MARCADORES BIOLOGICOS | es |
dc.title | Reduced necrosis and content of apoptotic M1 macrophages in advanced atherosclerotic plaques of mice with macrophage-specific loss of Trpc3 | es |
dc.type | Artículo | es |
dc.identifier.doi | 10.1038/srep42526 | - |
dc.identifier.pmid | 28186192 | - |
uca.disciplina | MUSICA | es |
uca.issnrd | 1 | es |
uca.affiliation | Fil: Solanki, Sumeet. University of Toledo. College of Medicine and Life Sciences. Department of Physiology and Pharmacology. Center for Hypertension and Personalized Medicine; Estados Unidos | es |
uca.affiliation | Fil: Dube, Prabhatchandra R. University of Toledo. College of Medicine and Life Sciences. Department of Physiology and Pharmacology. Center for Hypertension and Personalized Medicine; Estados Unidos | 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. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina | es |
uca.affiliation | Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences. Laboratory of Neurobiology; Estados Unidos | es |
uca.affiliation | Fil: Vazquez, Guillermo. University of Toledo. College of Medicine and Life Sciences. Department of Physiology and Pharmacology. Center for Hypertension and Personalized Medicine; Estados Unidos | es |
uca.version | publishedVersion | es |
item.grantfulltext | open | - |
item.fulltext | With Fulltext | - |
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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