Web of Science: 5 cites, Scopus: 5 cites, Google Scholar: cites,
Cardiomyocyte hypertrophy induced by Endonuclease G deficiency requires reactive oxygen radicals accumulation and is inhibitable by the micropeptide humanin
Blasco, Natividad (Cell Signaling and Apoptosis group, Universitat de Lleida - IRBLleida, Lleida, Spain)
Cámara, Yolanda (Research Group on Neuromuscular and Mitochondrial Diseases, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona and CIBERER, Barcelona, Spain)
Núñez, Estefanía (Cardiovascular Proteomics group, Spanish National Center for Cardiovascular Research (CNIC) and CIBERCV Madrid, Spain)
Beà, Aida (Cell Signaling and Apoptosis group, Universitat de Lleida - IRBLleida, Lleida, Spain)
Barés, Gisel (Cell Signaling and Apoptosis group, Universitat de Lleida - IRBLleida, Lleida, Spain)
Forné, Carles (Biostatistics Unit, IRBLleida, Universitat de Lleida, Lleida, Spain)
Ruíz-Meana, Marisol (Cardiovascular Diseases Research Group, VHIR and CIBERCV, Barcelona, Spain)
Girón, Cristina (Cell Signaling and Apoptosis group, Universitat de Lleida - IRBLleida, Lleida, Spain)
Barba, Ignasi (Cardiovascular Diseases Research Group, VHIR and CIBERCV, Barcelona, Spain)
García-Arumí, Elena (Research Group on Neuromuscular and Mitochondrial Diseases, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona and CIBERER, Barcelona, Spain)
García Dorado, David (Cardiovascular Diseases Research Group, VHIR and CIBERCV, Barcelona, Spain)
Vázquez, Jesús (Cardiovascular Proteomics group, Spanish National Center for Cardiovascular Research (CNIC) and CIBERCV Madrid, Spain)
Martí Seves, Ramon (Research Group on Neuromuscular and Mitochondrial Diseases, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona and CIBERER, Barcelona, Spain)
Llovera, Marta (Cell Signaling and Apoptosis group, Universitat de Lleida - IRBLleida, Lleida, Spain)
Sanchis, Daniel (Cell Signaling and Apoptosis group, Universitat de Lleida - IRBLleida, Lleida, Spain)

Data: 2018
Resum: The endonuclease G gene (Endog), which codes for a mitochondrial nuclease, was identified as a determinant of cardiac hypertrophy. How ENDOG controls cardiomyocyte growth is still unknown. Thus, we aimed at finding the link between ENDOG activity and cardiomyocyte growth. Endog deficiency induced reactive oxygen species (ROS) accumulation and abnormal growth in neonatal rodent cardiomyocytes, altering the AKT-GSK3β and Class-II histone deacethylases (HDAC) signal transduction pathways. These effects were blocked by ROS scavengers. Lack of ENDOG reduced mitochondrial DNA (mtDNA) replication independently of ROS accumulation. Because mtDNA encodes several subunits of the mitochondrial electron transport chain, whose activity is an important source of cellular ROS, we investigated whether Endog deficiency compromised the expression and activity of the respiratory chain complexes but found no changes in these parameters nor in ATP content. MtDNA also codes for humanin, a micropeptide with possible metabolic functions. Nanomolar concentrations of synthetic humanin restored normal ROS levels and cell size in Endog -deficient cardiomyocytes. These results support the involvement of redox signaling in the control of cardiomyocyte growth by ENDOG and suggest a pathway relating mtDNA content to the regulation of cell growth probably involving humanin, which prevents reactive oxygen radicals accumulation and hypertrophy induced by Endog deficiency.
Nota: Altres ajuts: Marató TV3 (20153810)
Nota: Número d'acord de subvenció MINECO/SAF2013–44942R
Nota: Número d'acord de subvenció ISCIII/RD12/0042/0035
Nota: Número d'acord de subvenció ISCIII/RD12/0042/0056
Nota: Número d'acord de subvenció ISCIII/RD12/0042/0021
Nota: Número d'acord de subvenció AGAUR/2009SGR-346
Drets: Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial i la comunicació pública de l'obra, sempre que no sigui amb finalitats comercials, i sempre que es reconegui l'autoria de l'obra original. No es permet la creació d'obres derivades. Creative Commons
Llengua: Anglès.
Document: article ; recerca ; publishedVersion
Matèria: Cardiac hypertrophy ; ENDOG ; Mitochondrial DNA ; Humanin
Publicat a: Redox biology, Vol. 16 (march 2018) , p. 146-156, ISSN 2213-2317

PMID: 29502044
DOI: 10.1016/j.redox.2018.02.021


11 p, 1.0 MB

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 Registre creat el 2018-06-18, darrera modificació el 2019-11-06



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