The autophagic degradation of Cav-1 contributes to PA-induced apoptosis and inflammation of astrocytes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-07

AUTHORS

Zi Chen, Sheng-Dan Nie, Min-Li Qu, Di Zhou, Liang-Yan Wu, Xia-Jie Shi, Ling-Ran Ma, Xin Li, Shan-Lei Zhou, Shan Wang, Jing Wu

ABSTRACT

The accumulation of palmitic acid (PA), implicated in obesity, can induce apoptotic cell death and inflammation of astrocytes. Caveolin-1 (Cav-1), an essential protein for astrocytes survival, can be degraded by autophagy, which is a double-edge sword that can either promote cell survival or cell death. The aim of this study was to delineate whether the autophagic degradation of Cav-1 is involved in PA-induced apoptosis and inflammation in hippocampal astrocytes. In this study we found that: (1) PA caused apoptotic death and inflammation by autophagic induction; (2) Cav-1 was degraded by PA-induced autophagy and PA induced autophagy in a Cav-1-independent manner; (3) the degradation of Cav-1 was responsible for PA-induced autophagy-dependent apoptotic cell death and inflammation; (4) chronic high-fat diet (HFD) induced Cav-1 degradation, apoptosis, autophagy, and inflammation in the hippocampal astrocytes of rats. Our results suggest that the autophagic degradation of Cav-1 contributes to PA-induced apoptosis and inflammation of astrocytes. Therefore, Cav-1 may be a potential therapeutic target for central nervous system injuries caused by PA accumulation. More... »

PAGES

771

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41419-018-0795-3

DOI

http://dx.doi.org/10.1038/s41419-018-0795-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1105413224

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29991726


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