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miR-27 regulates mitochondrial networks by directly targeting the mitochondrial fission factor

Mitochondrial morphology is dynamically regulated by forming small, fragmented units or interconnected networks, and this is a pivotal process that is used to maintain mitochondrial homeostasis. Although dysregulation of mitochondrial dynamics is related to the pathogenesis of several human diseases...

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Detalles Bibliográficos
Autores principales: Tak, Hyosun, Kim, Jihye, Jayabalan, Aravinth Kumar, Lee, Heejin, Kang, Hoin, Cho, Dong-Hyung, Ohn, Takbum, Nam, Suk Woo, Kim, Wook, Lee, Eun Kyung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4261914/
https://www.ncbi.nlm.nih.gov/pubmed/25431021
http://dx.doi.org/10.1038/emm.2014.73
Descripción
Sumario:Mitochondrial morphology is dynamically regulated by forming small, fragmented units or interconnected networks, and this is a pivotal process that is used to maintain mitochondrial homeostasis. Although dysregulation of mitochondrial dynamics is related to the pathogenesis of several human diseases, its molecular mechanism is not fully elucidated. In this study, we demonstrate the potential role of miR-27 in the regulation of mitochondrial dynamics. Mitochondrial fission factor (MFF) mRNA is a direct target of miR-27, whose ectopic expression decreases MFF expression through binding to its 3′-untranslated region. Expression of miR-27 results in the elongation of mitochondria as well as an increased mitochondrial membrane potential and mitochondrial ATP level. Our results suggest that miR-27 is a novel regulator affecting morphological mitochondrial changes by targeting MFF.