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

  • Neural Plast. 2021 Oct 4:2021:8851327. doi: 10.1155/2021/8851327.
Xiangli Xue  1  2 ,  Feng Li  3 ,  Ming Cai  4 ,  Jingyun Hu  1 ,  Qian Wang  1 ,  Shujie Lou  1  2
Affiliations
  • 1. Key Laboratory of Exercise and Health Sciences of Ministry of Education, Shanghai University of Sport, Shanghai, China.
  • 2. Shanghai Frontiers Science Research Base of Exercise and Metabolic Health, China.
  • 3. College of Physical Education, Guangxi University of Science and Technology, Liuzhou, China.
  • 4. College of Rehabilitation Sciences, Shanghai University of Medicine & Health Sciences, Shanghai, China.
PMID: 34646319 DOI: 10.1155/2021/8851327
Abstract

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.

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