RT Conference Proceedings
T1 IGF-II as a neuroprotective and neuroplastic factor in an oxidative damage model induced by glucocorticoids
T2 IGF-II  como factor neuroprotector y neuroplástico en un modelo de daño oxidativo
A1 Lara Fernández, Estrella
A1 Valverde, Nadia
A1 De Luque, Vanessa
A1 Boraldi, Federica
A1 Santín-Núñez, Luis Javier
A1 Pavía-Molina, José
A1 Martín-Montañez, Elisa
A1 García-Fernández, María Inmaculada
K1 Fisiología
AB IGF-II is a pleiotropic hormone widely distributed in the CNS, whichtriggers its functions by binding to IGF-IR, InsulinR and IGFII / M6P(IGF-IIR) receptors. Recently, it has been proposed that the effects ofIGF-II, interacting with IGF-IIR, are relevant not only for metabolism,growth and development, but also for neurotransmitter release, memoryconsolidation and neuroprotection under neurodegenerative processes.The results of our research group prove that IGF-II exerts metabolic,antioxidant and neuroprotective effects in aging. In relation toglucocorticoids, it has been revealed that the exposure of neural cells tohigh levels or prolonged incubation periods, produce synaptic alteration,neurodegeneration and neuronal death. Mechanisms of glucocorticoiddamageare mediated by oxidative stress induced by an increase in ROS,mitochondrial damage, decrease in antioxidant defenses, lipid andprotein membrane damage, etc. AIM: To study the antioxidant andneuroprotective effect of IGF-II in a model of oxidative damage inducedby glucocorticoids in aging. Results:Incubation of cells with CORT triggers oxidative damage, consumingantioxidant status. This oxidative stress produces damage andmitochondrial redistribution inducing synaptic changes, as shown thedecrease in synaptophysin and PSD95 levels together with a decrease inthe uptake and release of FM1-43, which may result inneurodegeneration. Incubation with IGF-II reverses these deleteriouseffects. Conclusions: Treatment of cells with IGF-II recovers thedamage produced by CORT, restoring synaptic function and decreasingneurodegeneration. These outcomes can be attributed to an antioxidanteffect mediated by the interaction of IGF-II with its specific IGF-IIR,which in turn mediates recovery of the redox balance via inhibition ofROS production, improvement of mitochondrial membrane potential /distribution and / or regulation of synaptic proteins.
YR 2018
FD 2018-10-11
LK https://hdl.handle.net/10630/16601
UL https://hdl.handle.net/10630/16601
LA eng
NO Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech, IBIMA
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 20 ene 2026