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Title 

Naloxone induces endoplasmic reticulum stress in PC12 cells

Authors 

S SeoY S KwonKweon YuS W KimO Y KwonK H KangK Kwon

Publisher 

Spandidos Publications

Issue Date 

2014

Citation 

Molecular Medicine Reports, vol. 9, no. 0, pp. 1395-1399

Keywords 

Endoplasmic reticulum chaperonesEndoplasmic reticulum stressNaloxone

Abstract 

Naloxone is an opioid inverse agonist used in the treatment of opiate overdose, with well known pharmacology. In the present study, we determined the effects of naloxone on the unfolded protein response (UPR) in PC12 cells. Data from a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay indicated that naloxone may accelerate PC12 cell apoptosis in a dose-dependent manner. We also demonstrated that naloxone upregulated gene expression of endoplasmic reticulum (ER) chaperones, including binding immunoglobulin protein (Bip), calnexin, ER protein 29 (ERp29) and protein disulfide isomerase (PDI), and ER stress sensors, including activating transcription factor 6 (ATF6), inositol-requiring enzyme 1 (IRE1) and protein kinase-like ER kinase (PERK). In addition, naloxone also induced typical ER stress phenomena, including ART6 proteolytic cleavage, eIF2α phosphorylation and XBP1 mRNA splicing. Furthermore, naloxone upregulated gene expression of ER chaperones and ER stress sensors in in vivo experiments. To the best of our knowledge, these results are the first to indicate that naloxone induces ER stress in vitro and in vivo.

ISSN 

1791-2997

Link 

http://dx.doi.org/10.3892/mmr.2014.1935

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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