NDLI: Endoplasmic reticulum stress preconditioning antagonizes low-density lipoprotein-induced inflammation in human mesangial cells through upregulation of XBP1 and suppression of the IRE1 /IKK/NF-κB pathway.

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Endoplasmic reticulum stress preconditioning antagonizes low-density lipoprotein-induced inflammation in human mesangial cells through upregulation of XBP1 and suppression of the IRE1 /IKK/NF-κB pathway.

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Endoplasmic reticulum stress preconditioning antagonizes low-density lipoprotein-induced inflammation in human mesangial cells through upregulation of XBP1 and suppression of the IRE1 /IKK/NF-κB pathway.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sun, Hang Zhang, Ling Yu, Yuan Tang, Lin Guo, Hui Liu, Qi
Description	Author Affiliation: Yu Y ( Department of Nephrology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, P.R. China.); Zhang L ( Department of Nephrology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, P.R. China.); Liu Q ( Institute for Viral Hepatitis, Key Laboratory of Molecular Biology for Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, P.R. China.); Tang L ( Department of Nephrology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, P.R. China.); Sun H ( Institute for Viral Hepatitis, Key Laboratory of Molecular Biology for Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, P.R. China.); Guo H ( Institute for Viral Hepatitis, Key Laboratory of Molecular Biology for Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, P.R. China.)
Abstract	Elevated plasma lowdensity lipoprotein (LDL) is associated with systemic inflammation, and is an important factor in the pathogenesis of chronic kidney disease. The aim of the present study was to investigate the effects of endoplasmic reticulum (ER) stress preconditioning on LDLinduced inflammatory responses, in human mesangial cells (HMCs). HMCs were exposed to LDL (200 nm), with or without pretreatment with tunicamycin, an ER stress inducer, and tested for changes to gene expression levels. Small interfering RNA technology was used to knockdown the expression of inositolrequiring enzyme1 (IRE1 ) and Xboxbinding protein1 (XBP1), in order to determine their effects on LDLtreated HMCs. LDL treatment resulted in a significant, and timedependent, increase in the relative mRNA expression levels of proinflammatory cytokines and CD40, which was coupled with enhanced phosphorylation of IRE1 , IκB kinase (IKK), and nuclear factor (NF)κB p65 and p65 nuclear translocation. The LDLinduced inflammatory responses were significantly reduced in the IRE1 depleted HMCs. Furthermore, pretreatment with tunicamycin significantly attenuated the induction of proinflammatory cytokines and CD40, by LDL. Whereas, silencing XBP1 expression significantly restored the production of proinflammatory cytokines, in the LDLtreated HMCs with ER stress preconditioning. The phosphorylation levels of IRE1 , IKK, and NFκB p65 were markedly increased in the XBP1depleted HMCs. Conversely, overexpression of XBP1 blocked LDLinduced inflammation in the HMCs. The results of the present study demonstrate that ER stress preconditioning antagonizes LDLinduced inflammatory responses in HMCs, which may be mediated through upregulation of XBP1, and subsequent inactivation of the IRE1 /IKK/NFκB pathway.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	3
Volume Number	11
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-03-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Dna-binding Proteins Metabolism Endoplasmic Reticulum Stress Endoribonucleases I-kappa B Kinase Inflammation Lipoproteins, Ldl Mesangial Cells Nf-kappa B Protein-serine-threonine Kinases Transcription Factors Antigens, Cd40 Genetics Cells, Cultured Cytokines Gene Expression Gene Silencing Inflammation Mediators Pharmacology Drug Effects Pathology Signal Transduction Tunicamycin Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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