eNOS-dependent S-nitrosylation of the NF-κB subunit p65 has neuroprotective effects

Ariel Caviedes, Barbara Maturana, Katherina Corvalán, Alexander Engler, Felipe Gordillo, Manuel Varas-Godoy, Karl Heinz Smalla, Luis Federico Batiz, Carlos Lafourcade, Thilo Kaehne, Úrsula Wyneken

Resultado de la investigación: Contribución a una revistaArtículorevisión exhaustiva

1 Cita (Scopus)

Resumen

Cell death by glutamate excitotoxicity, mediated by N-methyl-d-aspartate (NMDA) receptors, negatively impacts brain function, including but not limited to hippocampal neurons. The NF-κB transcription factor (composed mainly of p65/p50 subunits) contributes to neuronal death in excitotoxicity, while its inhibition should improve cell survival. Using the biotin switch method, subcellular fractionation, immunofluorescence, and luciferase reporter assays, we found that NMDA-stimulated NF-κB activity selectively in hippocampal neurons, while endothelial nitric oxide synthase (eNOS), an enzyme expressed in neurons, is involved in the S-nitrosylation of p65 and consequent NF-κB inhibition in cerebrocortical, i.e., resistant neurons. The S-nitro proteomes of cortical and hippocampal neurons revealed that different biological processes are regulated by S-nitrosylation in susceptible and resistant neurons, bringing to light that protein S-nitrosylation is a ubiquitous post-translational modification, able to influence a variety of biological processes including the homeostatic inhibition of the NF-κB transcriptional activity in cortical neurons exposed to NMDA receptor overstimulation.

Idioma originalInglés
Número de artículo4
Páginas (desde-hasta)4
PublicaciónCell Death and Disease
Volumen12
N.º1
DOI
EstadoPublicada - 4 ene 2021

Nota bibliográfica

Publisher Copyright:
© 2021, The Author(s).

Huella

Profundice en los temas de investigación de 'eNOS-dependent S-nitrosylation of the NF-κB subunit p65 has neuroprotective effects'. En conjunto forman una huella única.

Citar esto