RT Conference Proceedings
T1 Role of Insulin-Growth Factor II on mitochondrial recovery in a cellular model of Parkinson's Disease
A1 Valverde, Nadia
A1 Romero-Zerbo, Silvana Yanina
A1 Lara, Estrella
A1 Claros-Gil, Silvia
A1 Pavía-Molina, José
A1 Martín-Montañez, Elisa
A1 García-Fernández, María Inmaculada
K1 Parkinson, Enfermedad de - Congresos
K1 Patología mitocondrial - Congresos
K1 Insulina - Congresos
AB 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.
PB Journal of Physiology and Biochemistry
YR 2022
FD 2022-09
LK https://hdl.handle.net/10630/25097
UL https://hdl.handle.net/10630/25097
LA eng
NO Supported by M.G-F.&L.J.S. Proyectos I+D+I-Programa Operativo-FEDER Andalucía 2014-2020 (UMA18-FEDERJA-004) Junta de Andalucía.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 19 ene 2026