Artículo
Mitochondrial stress triggers a pro-survival response through epigenetic modifications of nuclear DNA
Mayorga, Lía
; Salassa, Betiana Nebaí
; Marzese, Diego Matías
; Loos, Mariana; Eiroa, Hernán D.; Lubieniecki, Fabiana; Garcia Samartino, Clara
; Romano, Patricia Silvia
; Roque Moreno, Maria
Fecha de publicación:
04/2019
Editorial:
Springer
Revista:
Cellular and Molecular Life Sciences
ISSN:
1420-682X
Idioma:
Inglés
Tipo de recurso:
Artículo publicado
Clasificación temática:
Resumen
Mitochondrial dysfunction represents an important cellular stressor and when intense and persistent cells must unleash an adaptive response to prevent their extinction. Furthermore, mitochondria can induce nuclear transcriptional changes and DNA methylation can modulate cellular responses to stress. We hypothesized that mitochondrial dysfunction could trigger an epigenetically mediated adaptive response through a distinct DNA methylation patterning. We studied cellular stress responses (i.e., apoptosis and autophagy) in mitochondrial dysfunction models. In addition, we explored nuclear DNA methylation in response to this stressor and its relevance in cell survival. Experiments in cultured human myoblasts revealed that intense mitochondrial dysfunction triggered a methylation-dependent pro-survival response. Assays done on mitochondrial disease patient tissues showed increased autophagy and enhanced DNA methylation of tumor suppressor genes and pathways involved in cell survival regulation. In conclusion, mitochondrial dysfunction leads to a “pro-survival” adaptive state that seems to be triggered by the differential methylation of nuclear genes.
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Articulos(IHEM)
Articulos de INST. HISTOLOGIA Y EMBRIOLOGIA DE MEND DR.M.BURGOS
Articulos de INST. HISTOLOGIA Y EMBRIOLOGIA DE MEND DR.M.BURGOS
Citación
Mayorga, Lía; Salassa, Betiana Nebaí; Marzese, Diego Matías; Loos, Mariana; Eiroa, Hernán D.; et al.; Mitochondrial stress triggers a pro-survival response through epigenetic modifications of nuclear DNA; Springer; Cellular and Molecular Life Sciences; 76; 7; 4-2019; 1397-1417
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