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Neuroinflammation alters cellular proteostasis by producing endoplasmic reticulum stress, autophagy activation and disrupting ERAD activation

Opened Access Neuroinflammation alters cellular proteostasis by producing endoplasmic reticulum stress, autophagy activation and disrupting ERAD activation

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Autor: Pintado Losa, Cristina
Macías, Sandra
Domínguez Martín, Helena
Castaño Navarro, Angélica
Ruano Caballero, Diego
Departamento: Universidad de Sevilla. Departamento de Bioquímica y Biología Molecular
Fecha: 2017
Publicado en: Scientific Reports, 7 (8100), 1-12.
Tipo de documento: Artículo
Resumen: Proteostasis alteration and neuroinflammation are typical features of normal aging. We have previously shown that neuroinflammation alters cellular proteostasis through immunoproteasome induction, leading to a transient decrease of proteasome activity. Here, we further investigated the role of acute lipopolysaccharide (LPS)-induced hippocampal neuroinflammation in cellular proteostasis. In particular, we focused on macroautophagy (hereinafter called autophagy) and endoplasmic reticulum-associated protein degradation (ERAD). We demonstrate that LPS injection induced autophagy activation that was dependent, at least in part, on glycogen synthase kinase (GSK)-3β activity but independent of mammalian target of rapamycin (mTOR) inhibition. Neuroinflammation also produced endoplasmic reticulum (ER) stress leading to canonical unfolded protein response (UPR) activation with a rapid activating transcription factor (ATF) 6α attenuation that resulted in a time-dependent down-regulation of ERAD ...
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Cita: Pintado Losa, C., Macías, S., Domínguez Martín, H., Castaño Navarro, A. y Ruano Caballero, D. (2017). Neuroinflammation alters cellular proteostasis by producing endoplasmic reticulum stress, autophagy activation and disrupting ERAD activation. Scientific Reports, 7 (8100), 1-12.
Tamaño: 2.056Mb
Formato: PDF

URI: http://hdl.handle.net/11441/64532

DOI: 10.1038/s41598-017-08722-3

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