Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/8529
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dc.contributor.authorHe, Xijues
dc.contributor.authorLi, Shoutianes
dc.contributor.authorLiu, Benjues
dc.contributor.authorSusperreguy, Sebastiánes
dc.contributor.authorFormoso, Karinaes
dc.contributor.authorYao, Jinghonges
dc.contributor.authorKang, Jinsonges
dc.contributor.authorAnbing, Shies
dc.contributor.authorBirnbaumer, Lutzes
dc.contributor.authorLiao, Yanhonges
dc.date.accessioned2019-08-01T01:37:29Z-
dc.date.available2019-08-01T01:37:29Z-
dc.date.issued2017-
dc.identifier.citationXiju, H., et. al. Major contribution of the 3/6/7 class of TRPC channels to myocardial ischemia/reperfusion and cellular hypoxia/reoxygenation injuries [en línea]. Proceedings of the National Academy of Sciences. 2017, 114 (23). doi:10.1073/pnas.1621384114. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8529es
dc.identifier.issn0027-8424 (impreso)-
dc.identifier.issn1091-6490 (online)-
dc.identifier.urihttps://repositorio.uca.edu.ar/handle/123456789/8529-
dc.identifier.urihttps://www.pnas.org/content/114/23/E4582-
dc.description.abstractAbstract: The injury phase after myocardial infarcts occurs during reperfusion and is a consequence of calcium release from internal stores combined with calcium entry, leading to cell death by apoptopic and necrotic processes. The mechanism(s) by which calcium enters cells has(ve) not been identified. Here, we identify canonical transient receptor potential channels (TRPC) 3 and 6 as the cation channels through which most of the damaging calcium enters cells to trigger their death, and we describe mechanisms activated during the injury phase. Working in vitro with H9c2 cardiomyoblasts subjected to 9-h hypoxia followed by 6-h reoxygenation (H/R), and analyzing changes occurring in areas-at-risk (AARs) of murine hearts subjected to a 30-min ischemia followed by 24-h reperfusion (I/R) protocol, we found: (i) that blocking TRPCwith SKF96365 significantly ameliorated damage induced by H/R, including development of the mitochondrial permeability transition and proapoptotic changes in Bcl2/BAX ratios; and (ii) that AAR tissues had increased TUNEL+ cells, augmented Bcl2/BAX ratios, and increased p(S240)NFATc3, p(S473) AKT, p(S9)GSK3β, and TRPC3 and -6 proteins, consistent with activation of a positive-feedback loop in which calcium entering through TRPCs activates calcineurin-mediated NFATc3-directed transcription of TRPC genes, leading to more Ca2+ entry. All these changes were markedly reduced in mice lacking TRPC3, -6, and -7. The changes caused by I/R in AAR tissues were matched by those seen after H/R in cardiomyoblasts in all aspects except for p-AKT and p-GSK3β, which were decreased after H/R in cardiomyoblasts instead of increased. TRPC should be promising targets for pharmacologic intervention after cardiac infarcts.es
dc.formatapplication/pdfes
dc.language.isoenges
dc.publisherNational Academy of Scienceses
dc.rightsAcceso Abiertoes
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/4.0/es
dc.sourceProceedings of the National Academy of Sciences 2017, 114 (23)es
dc.sourceISSN 0027-8424 (impreso)es
dc.sourceISSN 1091-6490 (online)es
dc.subjectINFARTO DEL MIOCARDIOes
dc.subjectCALCIOes
dc.subjectAPOPTOSISes
dc.subjectMUERTE CELULARes
dc.titleMajor contribution of the 3/6/7 class of TRPC channels to myocardial ischemia/reperfusion and cellular hypoxia/reoxygenation injurieses
dc.typeArtículoes
uca.pathFacultad de Ciencias Médicas|Instituto de Investigaciones Biomédicas (BIOMED UCA-CONICET)|Artículoses
uca.disciplinaMEDICINAes
uca.filename/home/data-uca-generic/folder_facultad/major-contribution-367-class/metadata.xmles
uca.issnrd1es
uca.affiliationFil: He, Xiju. Huazhong University of Science and Technology. Tongji Medical College. Department of Anatomy; Chinaes
uca.affiliationFil: He, Xiju. Huazhong University of Science and Technology. Tongji Medical College. Institute of Brain Research; Chinaes
uca.affiliationFil: He, Xiju. Hubei University of Medicine. Department of Anatomy; Chinaes
uca.affiliationFil: Li, Shoutian. Huazhong University of Science and Technology. Tongji Medical College. Department of Anatomy; Chinaes
uca.affiliationFil: Li, Shoutian. Huazhong University of Science and Technology. Tongji Medical College. Institute of Brain Research; Chinaes
uca.affiliationFil: Liu, Benju. Huazhong University of Science and Technology. Tongji Medical College. Department of Anatomy; Chinaes
uca.affiliationFil: Liu, Benju. Huazhong University of Science and Technology. Tongji Medical College. Institute of Brain Research; Chinaes
uca.affiliationFil: Susperreguy, Sebastian. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentinaes
uca.affiliationFil: Formoso, Karina. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentinaes
uca.affiliationFil: Yao, Jinghong. Huazhong University of Science and Technology. Tongji Medical College. Union Hospital. Department of Infectious Disease; Chinaes
uca.affiliationFil: Kang, Jinsong. Huazhong University of Science and Technology. Tongji Medical College. Tongji Hospital. Department of Surgery; Chinaes
uca.affiliationFil: Anbing, Shi. Huazhong University of Science and Technology. Tongji Medical College. Department of Biochemistry and Molecular Biology; Chinaes
uca.affiliationFil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentinaes
uca.affiliationFil: Birnbaumer, Lutz. Research Triangle Park. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados Unidoses
uca.affiliationFil: Liao, Yanhong. Huazhong University of Science and Technology. Tongji Medical College. Department of Anatomy; Chinaes
uca.affiliationFil: Liao, Yanhong. Huazhong University of Science and Technology. Tongji Medical College. Institute of Brain Research; Chinaes
uca.versionpublishedVersiones
item.languageiso639-1en-
item.grantfulltextopen-
item.fulltextWith Fulltext-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Función y Farmacología de Canales Iónicos-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Función y Farmacología de Canales Iónicos-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Función y Farmacología de Canales Iónicos-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.orcid0000-0002-0775-8661-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
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