IRIBARREN PABLO
Congresos y reuniones científicas
Título:
Autophagy modulates pro-inflammatory mediators in BV2 microglial cells and rescues both LPS and alpha-synuclein-induced neuronal cell death.
Autor/es:
BUSSI, C; PERALTA RAMOS, JM; GAVIGLIO, EA; ARROYO, DS; GALLEA, JI; CELEJ, MS; IRIBARREN, P
Lugar:
Londres
Reunión:
Congreso; Meeting of British Society for Cell Biology; 2015
Institución organizadora:
British Society for Cell Biology
Resumen:

Abstract:Autophagy is a fundamental cellular homeostatic mechanism, whereby cellsautodigest parts of their cytoplasm for removal or turnover. Despite theincreasing reports studying the effects of autophagy in the CNS, slightlyemphasis is placed on microglial cells.

The aim ofthis study was to evaluate the effects of autophagy on the production ofpro-inflammatory mediators by BV2 microglial cells, and on neuronal viabilityin a co-culture model. Autophagy was induced before or after TLR stimulation byrapamycin or trehalose and blocked by using 3-Methyladenine. Autophagyinduction in BV2 cells before LPS or alpha-synuclein stimulation downregulatedIL1b, IL-6, TNFa and nitric oxide production.

Furthermore,we observed in BV2/N2A co-cultures stimulated with LPS or alpha-synucleinfibers that induction of autophagy in microglial cells rescued LPS andalpha-synuclein-induced neuronal cell death.

Theseresults suggest that modulation of microglial cells by autophagy could be animportant strategy in the context of neurodegenerative diseases.