Regulated Necrosis Orchestrates Microglial Cell Death in Manganese-Induced Toxicity

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Microglia, the brain resident immune cells, play prominent roles in immune surveillance, tissue repair and neural regeneration. Despite these pro-survival actions, the relevance of these cells in the progression of several neuropathologies has been established. In the context of manganese (Mn) overe...

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Autor principal: Porte Alcon, S.
Otros Autores: Gorojod, R.M, Kotler, M.L
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Publicado: Elsevier Ltd 2018
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Biblioteca Central Dr. Luis F. Leloir (FCEN) de Universidad de Buenos Aires
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024 7 |2 cas  |a cathepsin D, 9025-26-7; manganese, 16397-91-4, 7439-96-5; Manganese; Reactive Oxygen Species 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a NRSCD 
100 1 |a Porte Alcon, S. 
245 1 0 |a Regulated Necrosis Orchestrates Microglial Cell Death in Manganese-Induced Toxicity 
260 |b Elsevier Ltd  |c 2018 
270 1 0 |m Kotler, M.L.Avda. Intendente Güiraldes 2160, Ciudad Universitaria, Argentina; email: kotler@qb.fcen.uba.ar 
506 |2 openaire  |e Política editorial 
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504 |a Zheng, H., Sun, H., Dominguez-Punaro, M.D.L.C., Bai, X., Ji, S., Segura, M., Xu, J., Evaluation of the pathogenesis of meningitis caused by Streptococcus suis sequence type 7 using the infection of BV2 microglial cells (2013) J Med Microbiol, 62, pp. 360-368 
520 3 |a Microglia, the brain resident immune cells, play prominent roles in immune surveillance, tissue repair and neural regeneration. Despite these pro-survival actions, the relevance of these cells in the progression of several neuropathologies has been established. In the context of manganese (Mn) overexposure, it has been proposed that microglial activation contributes to enhance the neurotoxicity. However, the occurrence of a direct cytotoxic effect of Mn on microglial cells remains controversial. In the present work, we investigated the potential vulnerability of immortalized mouse microglial cells (BV-2) toward Mn 2+ , focusing on the signaling pathways involved in cell death. Evidence obtained showed that Mn 2+ induces a decrease in cell viability which is associated with reactive oxygen species (ROS) generation. In this report we demonstrated, for the first time, that Mn 2+ triggers regulated necrosis (RN) in BV-2 cells involving two central mechanisms: parthanatos and lysosomal disruption. The occurrence of parthanatos is supported by several cellular and molecular events: (i) DNA damage; (ii) AIF translocation from mitochondria to the nucleus; (iii) mitochondrial membrane permeabilization; and (iv) PARP1-dependent cell death. On the other hand, Mn 2+ induces lysosomal membrane permeabilization (LMP) and cathepsin D (CatD) release into the cytosol supporting the lysosomal disruption. Pre-incubation with CatB and D inhibitors partially prevented the Mn 2+ -induced cell viability decrease. Altogether these events point to lysosomes as players in the execution of RN. In summary, our results suggest that microglial cells could be direct targets of Mn 2+ damage. In this scenario, Mn 2+ triggers cell death involving RN pathways. © 2018 IBRO  |l eng 
536 |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas, PIP 0771, 0519 
536 |a Detalles de la financiación: This work was supported by grants from the Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET, Grants PIP 0771 and 0519 ). The authors thank Dr. Alicia Baldessari (QO-FCEN-UBA, UMYMFOR-CONICET), Dr. Eduardo Canepa (QB-FCEN-UBA, IQUIBICEN-CONICET) and Dr. Nora Rotstein (BByF, UNS-INIBIBB-CONICET) for providing relevant materials. R.M.G. and S.P.A. are supported by a CONICET scholarships. M.L.K. is a researcher member at CONICET. 
593 |a CONICET-Universidad de Buenos Aires, Instituto de Química Biológica Ciencias Exactas y Naturales (IQUIBICEN), Facultad de Ciencias Exactas y Naturales, Departamento de Química Biológica, Laboratorio de Disfunción Celular en Enfermedades Neurodegenerativas y Nanomedicina, Buenos Aires, Argentina 
690 1 0 |a LYSOSOMES, REGULATED NECROSIS 
690 1 0 |a MANGANESE 
690 1 0 |a MANGANISM 
690 1 0 |a MICROGLIA 
690 1 0 |a PARTHANATOS 
690 1 0 |a CATHEPSIN D 
690 1 0 |a MANGANESE 
690 1 0 |a NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE 1 
690 1 0 |a REACTIVE OXYGEN METABOLITE 
690 1 0 |a MANGANESE 
690 1 0 |a ANIMAL CELL 
690 1 0 |a APOPTOSIS 
690 1 0 |a ARTICLE 
690 1 0 |a CELL DEATH 
690 1 0 |a CELL DISRUPTION 
690 1 0 |a CELL STRUCTURE 
690 1 0 |a CELL VIABILITY 
690 1 0 |a DNA DAMAGE 
690 1 0 |a GENOTOXICITY 
690 1 0 |a HUMAN 
690 1 0 |a HUMAN CELL 
690 1 0 |a LYSOSOME 
690 1 0 |a MICROGLIA 
690 1 0 |a MTT ASSAY 
690 1 0 |a NONHUMAN 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a SIGNAL TRANSDUCTION 
690 1 0 |a ANIMAL 
690 1 0 |a CELL DEATH 
690 1 0 |a CELL SURVIVAL 
690 1 0 |a DRUG EFFECT 
690 1 0 |a METABOLISM 
690 1 0 |a MICROGLIA 
690 1 0 |a MITOCHONDRION 
690 1 0 |a MOUSE 
690 1 0 |a ANIMALS 
690 1 0 |a APOPTOSIS 
690 1 0 |a CELL DEATH 
690 1 0 |a CELL SURVIVAL 
690 1 0 |a LYSOSOMES 
690 1 0 |a MANGANESE 
690 1 0 |a MICE 
690 1 0 |a MICROGLIA 
690 1 0 |a MITOCHONDRIA 
690 1 0 |a REACTIVE OXYGEN SPECIES 
650 1 7 |2 spines  |a NECROSIS 
650 1 7 |2 spines  |a NECROSIS 
700 1 |a Gorojod, R.M. 
700 1 |a Kotler, M.L. 
773 0 |d Elsevier Ltd, 2018  |g v. 393  |h pp. 206-225  |p Neuroscience  |x 03064522  |w (AR-BaUEN)CENRE-759  |t Neuroscience 
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856 4 0 |u https://doi.org/10.1016/j.neuroscience.2018.10.006  |y DOI 
856 4 0 |u https://hdl.handle.net/20.500.12110/paper_03064522_v393_n_p206_PorteAlcon  |y Handle 
856 4 0 |u https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03064522_v393_n_p206_PorteAlcon  |y Registro en la Biblioteca Digital 
961 |a paper_03064522_v393_n_p206_PorteAlcon  |b paper  |c PE 
962 |a info:eu-repo/semantics/article  |a info:ar-repo/semantics/artículo  |b info:eu-repo/semantics/publishedVersion 
963 |a VARI 
999 |c 85916 

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