New protein-protein interactions of mitochondrial connexin 43 in mouse heart
Denuc, Amanda (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Núñez, Estefanía (Centro de Investigación Biomédica en Red en Enfermedades Cardiovasculares)
Calvo, Enrique (Centro de Investigación Biomédica en Red en Enfermedades Cardiovasculares)
Loureiro, Marta (Centro de Investigación Biomédica en Red en Enfermedades Cardiovasculares)
Miro-Casas, Elisabet (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Guarás, Adela (Centro de Investigación Biomédica en Red en Enfermedades Cardiovasculares)
Vázquez, Jesús (Centro de Investigación Biomédica en Red en Enfermedades Cardiovasculares)
García-Dorado, David (Hospital Universitari Vall d'Hebron. Institut de Recerca)
Universitat Autònoma de Barcelona

Data:	2016
Resum:	Connexin 43 (Cx43), the gap junction protein involved in cell-to-cell coupling in the heart, is also present in the subsarcolemmal fraction of cardiomyocyte mitochondria. It has been described to regulate mitochondrial potassium influx and respiration and to be important for ischaemic preconditioning protection, although the molecular effectors involved are not fully characterized. In this study, we looked for potential partners of mitochondrial Cx43 in an attempt to identify new molecular pathways for cardioprotection. Mass spectrometry analysis of native immunoprecipitated mitochondrial extracts showed that Cx43 interacts with several proteins related with mitochondrial function and metabolism. Among them, we selected for further analysis only those present in the subsarcolemmal mitochondrial fraction and known to be related with the respiratory chain. Apoptosis-inducing factor () and the beta-subunit of the electron-transfer protein (), two proteins unrelated to date with Cx43, fulfilled these conditions, and their interaction with Cx43 was proven by direct and reverse co-immunoprecipitation. Furthermore, a previously unknown molecular interaction between and was established, and protein content and sub-cellular localization appeared to be independent from the presence of Cx43. Our results identify new protein-protein interactions between -Cx43, -Cx43 and - as possible players in the regulation of the mitochondrial redox state.
Ajuts:	Ministerio de Economía y Competitividad SAF 2008-03067 Instituto de Salud Carlos III RD12/0042/0021
Drets:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Llengua:	Anglès
Document:	Article ; recerca ; Versió publicada
Matèria:	Connexin 43 ; Apoptosis-inducing factor ; Electron-transfer protein ; Mitochondria ; Cardiomyocyte
Publicat a:	Journal of Cellular and Molecular Medicine, Vol. 20, issue 5 (May 2016) , p. 794-803, ISSN 1582-4934

DOI: 10.1111/jcmm.12792
PMID: 26915330

10 p, 749.9 KB

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