IQUIBICEN   23947
INSTITUTO DE QUIMICA BIOLOGICA DE LA FACULTAD DE CIENCIAS EXACTAS Y NATURALES
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Autophagy protects BV-2 microglial cells from manganese-induced cell death
Autor/es:
PORTE ALCÓN SOLEDAD; GOROJOD ROXANA MAYRA; KOTLER MÓNICA LIDIA
Lugar:
Mar del Plata
Reunión:
Congreso; Reunión anual de Sociedades Biocientíficas 2019; 2019
Institución organizadora:
SAIC, SAFE, SAB, SAP, NANOMED-ar, AACYTAL, HCS
Resumen:
Manganese (Mn) is a trace metal required for human health. As a micronutrient, Mn is needed only in small quantities and can become toxic at higher concentrations. Chronic exposure to Mn, in occupational or environmental settings, causes a parkinsonian-like syndrome known as Manganism. More than a century after its discovery, Mn neurotoxicity is still considered a public health concern. Like neurons, glial cells are susceptible to Mn-induced injury. We have previously demonstrated that Mn triggers microglial cell death by regulated necrosis, involving both parthanatos and lysosomal disruption. Autophagy is a catabolic pathway in which cellular components are degraded by lysosomes in response to stress conditions. Nevertheless, autophagy activation may have both beneficial and detrimental effects, depending on the context. Evidence indicates that Mn activates autophagy in microglial cells. However, the role of autophagy on microglial cell death remains unknown. To address this question, we exposed BV-2 cells to Mn and analyzed the time-course of autophagy activation and the effect of its modulation on cellular fate. We detected a time-dependent increase in LC3-II protein levels (WB and ICC; p