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SGK1.1 limits brain damage after status epilepticus through M current-dependent and independent mechanisms Martín Batista, Elva Maglio, Laura E. Armas Capote, Natalia Hernandez, Guadalberto Alvarez de la Rosa, Diego Giraldez, Teresa Abstract Epilepsy is a neurological condition associated to significant brain damage produced by status epilepticus (SE) including neurodegeneration, gliosis and ectopic neurogenesis. Reduction of these processes constitutes a useful strategy to improve recovery and ameliorate negative outcomes after an initial insult. SGK1.1, the neuronal isoform of the serum and glucocorticoids-regulated kinase 1 (SGK1), has been shown to increase M-current density in neurons, leading to reduced excitability and protection against seizures. For this study, we used 4-5 months old male transgenic C57BL/6 J and FVB/NJ mice expressing near physiological levels of a constitutively active form of the kinase controlled by its endogenous promoter. Here we show that SGK1.1 activation potently reduces levels of neuronal death (assessed using Fluoro-Jade C staining) and reactive glial activation (reported by GFAP and Iba-1 markers) in limbic regions and cortex, 72 h after SE induced by kainate, even in the context of high seizure activity. This neuroprotective effect is not exclusively through M-current activation but is also directly linked to decreased apoptosis levels assessed by TUNEL assays and quantification of Bim and Bcl-xL by western blot of hippocampal protein extracts. Our results demonstrate that this newly described antiapoptotic role of SGK1.1 activation acts synergistically with the regulation of cellular excitability, resulting in a significant reduction of SE-induced brain damage in areas relevant to epileptogenesis. 2025-12-15T13:00:00Z 2025-12-15T13:00:00Z 2021-06 journal article Martin-Batista, Elva, et al. «SGK1.1 Limits Brain Damage after Status Epilepticus through M Current-Dependent and Independent Mechanisms». Neurobiology of Disease, vol. 153, junio de 2021, p. 105317. https://doi.org/10.1016/j.nbd.2021.105317. 10.1016/j.nbd.2021.105317 https://hdl.handle.net/20.500.14352/128981 https://doi.org/10.1016/j.nbd.2021.105317 33639207 https://www.sciencedirect.com/science/article/pii/S0969996121000668 eng http://creativecommons.org/licenses/by-nc-nd/4.0/ open access Attribution-NonCommercial-NoDerivatives 4.0 International Elsevier