2026-05-27T04:50:08Zhttps://riuma.uma.es/rest/oai/requestoai:riuma.uma.es:10630/250972026-02-03T12:20:50Zcom_10630_2254col_10630_37959
RIUMA. Repositorio Institucional de la Universidad de Málaga
author
Valverde, Nadia
author
Romero-Zerbo, Silvana Yanina
author
Lara, Estrella
author
Claros-Gil, Silvia
author
Pavía-Molina, José
author
Martín-Montañez, Elisa
author
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
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
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URL
https://riuma.uma.es/bitstreams/7a58d0a3-77a6-4081-8b86-967a58bf0075/download
File
MD5
bfbf8cb0dab3b7f69ae690c850312169
1975266
application/pdf
SECF-Nadia Valverde.pdf