RT Journal Article
T1 SGK1.1 limits brain damage after status epilepticus through M current-dependent and independent mechanisms
A1 Martín Batista, Elva
A1 Maglio, Laura E.
A1 Armas Capote, Natalia
A1 Hernandez, Guadalberto
A1 Alvarez de la Rosa, Diego
A1 Giraldez, Teresa
AB AbstractEpilepsy 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.
PB Elsevier
YR 2021
FD 2021-06
LK https://hdl.handle.net/20.500.14352/128981
UL https://hdl.handle.net/20.500.14352/128981
LA eng
NO 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.
DS Docta Complutense
RD 25 feb 2026