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miR-16-5p Suppression Protects Human Cardiomyocytes against Endoplasmic Reticulum and Oxidative Stress-Induced Injury

Título : miR-16-5p Suppression Protects Human Cardiomyocytes against Endoplasmic Reticulum and Oxidative Stress-Induced Injury
Autor : Toro Cebada, Rocío
Perez-Serra, Alexandra
Mangas Rojas, Alipio
Campuzano, Oscar
Sarquella-Brugada, Georgia
Quezada‑Feijoo, Maribel
Ramos, Mónica
Alcalá Díaz-Mor, Martín
Carrera Puerta, Esther
García-Padilla, Carlos
Franco, Diego
Bonet Martínez, Fernando
Materias: miR-16-5pIschemic dilated cardiomyopathyReactive oxygen speciesEndoplasmic reticulum stressATF6
Editorial : MDPI
Citación : Toro, R.; Pérez-Serra, A.; Mangas, A.; Campuzano, O.; Sarquella-Brugada, G.; Quezada-Feijoo, M.; Ramos, M.; Alcalá, M.; Carrera, E.; García-Padilla, C.; et al.miR-16-5p Suppression Protects Human Cardiomyocytes against Endoplasmic Reticulumand Oxidative Stress-Induced Injury. Int. J. Mol. Sci. 2022, 23, 1036. https://doi.org/ 10.3390/ijms23031036
Resumen : Oxidative stress, defined as the excess production of reactive oxygen species (ROS) relative to antioxidant defense, plays a significant role in the development of cardiovascular diseases. Endoplasmic reticulum (ER) stress has emerged as an important source of ROS and its modulation could be cardioprotective. Previously, we demonstrated that miR-16-5p is enriched in the plasma of ischemic dilated cardiomyopathy (ICM) patients and promotes ER stress-induced apoptosis in cardiomyocytes in vitro. Here, we hypothesize that miR-16-5p might contribute to oxidative stress through ER stress induction and that targeting miR-16-5p may exert a cardioprotective role in ER stress-mediated cardiac injury. Analysis of oxidative markers in the plasma of ICM patients demonstrates that oxidative stress is associated with ICM. Moreover, we confirm that miR-16-5p overexpression promotes oxidative stress in AC16 cardiomyoblasts. We also find that, in response to tunicamycin-induced ER stress, miR-16-5p suppression decreases apoptosis, inflammation and cardiac damage via activating the ATF6-mediated cytoprotective pathway. Finally, ATF6 is identified as a direct target gene of miR-16-5p by dual-luciferase reporter assays. Our results indicate that miR-16-5p promotes ER stress and oxidative stress in cardiac cells through regulating ATF6, suggesting that the inhibition of miR-16-5p has potential as a therapeutic approach to protect the heart against ER and oxidative stress-induced injury.
URI : http://hdl.handle.net/10637/14697
Derechos: http://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
OpenAccess
ISSN : 1422-0067
Fecha de publicación : 18-ene-2022
Centro : Universidad San Pablo-CEU
Aparece en las colecciones: Facultad de Farmacia





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