RT Journal Article
T1 New molecular mechanisms to explain the neuroprotective effects of insulin-like growth factor II in a cellular model of Parkinson's disease
A1 Romero-Zerbo, Silvana Yanina
A1 Valverde, Nadia
A1 Claros-Gil, Silvia
A1 Zamorano-González, Pablo
A1 Boraldi, Federica
A1 Lofaro, Francesco-Demetrio
A1 Lara, Estrella
A1 Pavía-Molina, José
A1 García-Fernández, María Inmaculada
A1 Gago-Calderón, Belén
A1 Martín-Montañez, Elisa
K1 Parkinson, Enfermedad de
K1 Mitocondrias
K1 Ciclo celular
AB IntroductionOne of the hallmarks of Parkinsońs Disease (PD) is oxidative distress, leading to mitochondrial dysfunction and neurodegeneration. Insulin-like growth factor II (IGF-II) has been proven to have antioxidant and neuroprotective effects in some neurodegenerative diseases, including PD. Consequently, there is growing interest in understanding the different mechanisms involved in the neuroprotective effect of this hormone.ObjectivesTo clarify the mechanism of action of IGF-II involved in the protective effect of this hormone.MethodsThe present study was carried out on a cellular model PD based on the incubation of dopaminergic cells (SN4741) in a culture with the toxic 1-methyl-4-phenylpyridinium (MPP+), in the presence of IGF-II. This model undertakes proteomic analyses in order to understand which molecular cell pathways might be involved in the neuroprotective effect of IGF-II. The most important proteins found in the proteomic study were tested by Western blot, colorimetric enzymatic activity assay and immunocytochemistry. Along with the proteomic study, mitochondrial morphology and function were also studied by transmission electron microscopy and oxygen consumption rate. The cell cycle was also analysed using 7AAd/BrdU staining, and flow cytometry.ResultsThe results obtained indicate that MPP+, MPP++IGF-II treatment and IGF-II, when compared to control, modified the expression of 197, 246 proteins and 207 respectively. Some of these proteins were found to be involved in mitochondrial structure and function, and cell cycle regulation. Including IGF-II in the incubation medium prevents the cell damage induced by MPP+, recovering mitochondrial function and cell cycle dysregulation, and thereby decreasing apoptosis.
PB Elsevier
YR 2024
FD 2024-02-08
LK https://hdl.handle.net/10630/33547
UL https://hdl.handle.net/10630/33547
LA eng
NO Romero-Zerbo, S.-Y., Valverde, N., Claros, S., Zamorano-Gonzalez, P., Boraldi, F., Lofaro, F.-D., Lara, E., Pavia, J., Garcia-Fernandez, M., Gago, B., & Martin-Montañez, E. (2024). New molecular mechanisms to explain the neuroprotective effects of insulin-like growth factor II in a cellular model of Parkinson’s disease. Journal of Advanced Research.
NO Partial funding for open access charge: Universidad de Málaga / CBUA.  This research was supported by the following projects: M.G-F, E.M-M and SY.R-Z Plan Propio de la Universidad de Málaga 2022 (B4-2023-3, B1-2022-15 and C1) and Ministerio de Economía y Competitividad. Gobierno de España. (MINECO, Agencia Estatal de Investigación cofinanciado por FEDER-UE (PID2020-113806RB-I00) and; F.B “Fondazione Cassa di Risparmio di Modena” for funding use expenses of Talos F200S G2 transmission electron microscope and Q Exactive Hybrid Quadrupole-Orbitrap Mass Spectrometer at CIGS, UNIMORE. Partial funding for open access charge: Universidad de Málaga / CBUA.
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 21 ene 2026