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Beneficial effect of ER stress preconditioning in protection against FFA-induced adipocyte inflammation via XBP1 in 3T3-L1 adipocytes.

Authors
  • Wang, Min1
  • Chen, Xi2
  • Zheng, Zhenda1
  • Yu, Shujie1
  • Zhou, Bin1
  • Liu, Yong1
  • Liu, Dinghui1
  • Chen, Yanming3
  • Qian, Xiaoxian4, 5
  • 1 Department of Cardiology, The Third Affiliated Hospital of Sun Yat-sen University, Sun Yat-sen University, 600 Tianhe, Guangzhou, 510630, Guangdong, China. , (China)
  • 2 Department of Rehabilitation Medicine, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510630, Guangdong, China. , (China)
  • 3 Department of Endocrinology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510630, Guangdong, China. [email protected] , (China)
  • 4 Department of Cardiology, The Third Affiliated Hospital of Sun Yat-sen University, Sun Yat-sen University, 600 Tianhe, Guangzhou, 510630, Guangdong, China. [email protected] , (China)
  • 5 Institute Integrated Traditional Chinese and Western Medicine, Sun Yat-sen University, Guangzhou, 510630, Guangdong, China. [email protected] , (China)
Type
Published Article
Journal
Molecular and Cellular Biochemistry
Publisher
Springer-Verlag
Publication Date
Jan 01, 2020
Volume
463
Issue
1-2
Pages
45–55
Identifiers
DOI: 10.1007/s11010-019-03627-3
PMID: 31630283
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Adipose tissue inflammation is closely associated with the development of obesity and insulin resistance. Free fatty acids (FFAs) are a major inducer of obesity-related insulin resistance. Previously, we reported that endoplasmic reticulum (ER) stress potentially mediated retinal inflammation in diabetic retinopathy. The unfolded protein response (UPR) protects cells against damage induced by oxidative stress. X-box binding protein 1 (XBP1) plays a major role in protecting cells by modulating the UPR. However, the link between ER stress and adipocyte inflammation has been poorly investigated. In the present study, we found that pretreatment of 3T3-L1 adipocytes with a low dose of ER stress inducer tunicamycin inhibited FFA-induced upregulated expression of inflammatory cytokines. In addition, FFAs induced phosphorylation of the p65 subunit of NF-κB was largely inhibited by pretreatment with tunicamycin in 3T3-L1 adipocytes. Knockdown of XBP1 by siRNA markedly mitigated the protective effects of preconditioning against inflammation. Conversely, overexpression of XBP1 alleviated FFA-induced phosphorylation of IκB-α, IKKα/β, and NF-κB, which was accompanied by decreased inflammatory cytokine expression. Collectively, these results imply a beneficial role of ER stress preconditioning in protecting against FFA-induced 3T3-L1 adipocyte inflammation, which is likely mediated through inhibition of the IKK/NF-κB pathway via XBP1.

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