MiR-27b attenuates mitochondrial oxidative stress and inflammation in endothelial cells

• DOI: 10.1016/j.redox.2023.102681
• Publication Date: 2023-03-17T02:15:09Z
• Authors: Nunzia D'Onofrio; Francesco Prattic...; Elisa Martino; Camilla Anastasio; Luigi Mele; Rosalba La Grotta; Celestino Sardu; Antonio Ceriello; Raffaele Marfella; Giuseppe Paolisso; Maria Luisa Bales...
• Keywords: FOXO1; Mitochondrial ROS

MiR-27b is highly expressed in endothelial cells (EC) but its function this context poorly characterized. This study aims to investigate the effect of miR-27b on inflammatory pathways, cell cycle, apoptosis, and mitochondrial oxidative imbalances immortalized human aortic (teloHAEC), umbilical vein (HUVEC), coronary artery (HCAEC) exposed TNF-α. Treatment with TNF-α downregulates expression all EC lines, promotes activation induces alteration reactive oxygen species accumulation, fostering induction intrinsic apoptosis. Moreover, mimic counteracts TNF-α-related cytotoxicity inflammation, as well cycle arrest caspase-3-dependent restoring mitochondria redox state, function, membrane polarization. Mechanistically, hsa-miR-27b-3p targets 3'untranslated regions FOXO1 mRNA downregulate expression, blunting Akt/FOXO1 pathway. Here, we show that involved regulation a broad range functionally intertwined phenomena EC, suggesting key role mitigating mithochondrial stress most likely through targeting FOXO1. Overall, results reveal for first time could represent possible target future therapies aimed at improving health.