Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/14597
Título : CFTR chloride channel activity modulates the mitochondrial morphology in cultured epithelial cells
Autor : García Solcá, Rocío 
Falduti, Camila 
Clauzure, Mariángeles 
Jara, Raquel 
Massip Copiz, María M. 
Aguilar, María de los Angeles 
Santa Coloma, Tomás Antonio 
Valdivieso, Ángel Gabriel 
Palabras clave : FIBROSIS QUISTICADINAMICA MITOCONDRIALREGULADOR DE CONDUCTANCIA DE TRANSMEMBRANA DE FIBROSIS QUISTICACELULAS EPITELIALESDRP1MFN1Mdivi-1
Fecha de publicación : 2021
Editorial : Elsevier
Cita : García Solcá, R. et al. CFTR chloride channel activity modulates the mitochondrial morphology in cultured epithelial cells [en línea]. International Journal of Biochemistry and Cell Biology. 2021, 135, 105976. doi: 10.1016/j.biocel.2021.105976. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/14597
Resumen : Abstract: The impairment of the CFTR channel activity, a cAMP-activated chloride (Cl− ) channel responsible for cystic fibrosis (CF), has been associated with a variety of mitochondrial alterations such as modified gene expression, impairment in oxidative phosphorylation, increased reactive oxygen species (ROS), and a disbalance in calcium homeostasis. The mechanisms by which these processes occur in CF are not fully understood. Previously, we demonstrated a reduced MTND4 expression and a failure in the mitochondrial complex I (mCx-I) activity in CF cells. Here we hypothesized that the activity of CFTR might modulate the mitochondrial fission/fusion balance, explaining the decreased mCx-I. The mitochondrial morphology and the levels of mitochondrial dynamic proteins MFN1 and DRP1 were analysed in IB3− 1 CF cells, and S9 (IB3− 1 expressing wt-CFTR), and C38 (IB3− 1 expressing a truncated functional CFTR) cells. The mitochondrial morphology of IB3− 1 cells compared to S9 and C38 cells showed that the impaired CFTR activity induced a fragmented mitochondrial network with increased rounded mitochondria and shorter branches. Similar results were obtained by using the CFTR pharmacological inhibitors CFTR(inh)-172 and GlyH101 on C38 cells. These morphological changes were accompanied by modifications in the levels of the mitochondrial dynamic proteins MFN1, DRP1, and p(616)-DRP1. IB3− 1 CF cells treated with Mdivi-1, an inhibitor of mitochondrial fission, restored the mCx-I activity to values similar to those seen in S9 and C38 cells. These results suggest that the mitochondrial fission/fusion balance is regulated by the CFTR activity and might be a potential target to treat the impaired mCx-I activity in CF.
URI : https://repositorio.uca.edu.ar/handle/123456789/14597
ISSN : 1357-2725
Disciplina: MEDICINA
DOI: 10.1016/j.biocel.2021.105976
Derechos: Acceso restringido
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