2026-05-27T20:39:25Zhttps://riuma.uma.es/rest/oai/request

oai:riuma.uma.es:10630/250972026-02-03T12:20:50Zcom_10630_2254col_10630_37959

Valverde, Nadia Romero-Zerbo, Silvana Yanina Lara, Estrella Claros-Gil, Silvia Pavía-Molina, José Martín-Montañez, Elisa García-Fernández, María Inmaculada 2022-09-27T11:05:44Z 2022-09-27T11:05:44Z 2022-09 https://hdl.handle.net/10630/25097 Insulin-growth factor II (IGF-II) has shown antioxidant and neuroprotective effects in some neurodegenerative disorders. ROS causes damage to cellular macromolecules affecting several cellular processes and resulting in cell death. Mitochondrial ROS damage has a critical role in the pathobiology of PD. The objective was to assess the IGF-II role in the recovery of the oxidative damage produced on mitochondrial in a cellular model of PD. SN4741 cell line was treated as follows: MPP+ alone, in presence of IGF-II and/or co-incubated BMS (Ins/IGF-I receptors antagonist) or AB (anti-IGF-II-receptor). To assess the effect of IGF-II in the recovery of MPP+ damage, this treatment was removed after 2 h and replaced during another 2 h by medium, IGF-II or IGF-II + BMS or IGF-II + AB. Cell death was analysed through annexin-V Mitochondrial structure, localization and morphology was studied by western blot/ immunochemistry of Mitofilin (Mtf) and electron microscopy; function by Mitotracker and oxygen consumption rate. IGF-II prevented MPP+ cell death. In morphological/structural studies, MPP+ treated cells showed swollen mitochondria with loss of cristae, and electron-lucent matrix, inducing a mitochondrial number reduction. IGF-II retrieved normal-shaped mitochondria with intact cristae and outer/inner membranes. Moreover, MPP+ incubation significantly reduced the expression levels of Mtf compared to the CO. This expression was found in areas that had a very weak mark, indicating mitochondrial destruction or dysfunction. IGF-II coincubation, recovered the expression of Mtf, remaining associated with healthy mitochondrial function. Additionally, the decrease in OCR levels after MPP+ administration was recovered in presence of IGF-II. The BMS-receptor blockage did not modify the IGF-II responses, and AB limited its effect. In conclusion, IGF-II recovers mitochondrial structure and function due to MPP+ damage. This improvement is carried out through the specific IGF-II receptor. eng http://creativecommons.org/licenses/by-nc-nd/4.0/ open access Attribution-NonCommercial-NoDerivatives 4.0 Internacional Parkinson, Enfermedad de - Congresos Patología mitocondrial - Congresos Insulina - Congresos Role of Insulin-Growth Factor II on mitochondrial recovery in a cellular model of Parkinson's Disease conference output