Interactions between Endoplasmic Reticulum Stress and Autophagy Implications for Apoptosis and Neuroplasticity-Related Proteins in Palmitic Acid-Treated Prefrontal Cells

Interactions between Endoplasmic Reticulum Stress and Autophagy : Implications for Apoptosis and Neuroplasticity-Related Proteins in Palmitic Acid-Treated Prefrontal Cells

Copyright © 2021 Xiangli Xue et al.

Bibliographische Detailangaben
Veröffentlicht in:Neural plasticity. - 1998. - 2021(2021) vom: 11., Seite 8851327
1. Verfasser: Xue, Xiangli (VerfasserIn)
Weitere Verfasser: Li, Feng, Cai, Ming, Hu, Jingyun, Wang, Qian, Lou, Shujie
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2021
Zugriff auf das übergeordnete Werk:Neural plasticity
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Enzyme Inhibitors Palmitic Acid 2V16EO95H1
Beschreibung
Zusammenfassung:Copyright © 2021 Xiangli Xue et al.
Lipotoxicity of palmitic acid (PA) or high-fat diets has been reported to increase endoplasmic reticulum (ER) stress and autophagy in peripheral tissue as well as apoptotic cell death. It also can lead to an AD-like pathological pattern. However, it has been unknown that PA-induced ER stress and autophagy are involved in the regulation of neuroplastic abnormalities. Here, we investigated the roles of ER stress and autophagy in apoptosis and neuroplasticity-related protein expression in PA-treated prefrontal cells. Prefrontal cells dissected from newborn Sprague-Dawley rats were treated with PA compound with ER stress inhibitor 4-phenylbutyric acid (4-PBA) and autophagy inhibitor 3-methyladenine (3-MA) or PA alone. PA promoted ER stress and autophagy and also cause apoptosis as well as a decline in the expression of neuroplasticity-related proteins. Inhibition of ER stress decreased the expressions of neuroplasticity-related proteins and reduced autophagy activation and apoptosis in PA-treated prefrontal cells. Inhibition of autophagy exacerbated apoptosis and enhanced ER stress in PA-treated prefrontal cells. The present study illustrated that both ER stress and autophagy could be involved in apoptosis and decreased neuroplasticity-related proteins, and the interaction between ER stress and autophagy may play a critical role in apoptosis in PA-treated prefrontal cells. Our results provide new insights into the molecular mechanisms in vitro of lipotoxicity in obesity-related cognitive dysfunction
Beschreibung:Date Completed 02.03.2022
Date Revised 02.03.2022
published: Electronic-eCollection
Citation Status MEDLINE
ISSN:1687-5443
DOI:10.1155/2021/8851327