Naloxone induces endoplasmic reticulum stress in PC12 cells

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Title
Naloxone induces endoplasmic reticulum stress in PC12 cells
Author(s)
S Seo; Y S Kwon; Kweon Yu; S W Kim; O Y Kwon; K H Kang; K Kwon
Bibliographic Citation
Molecular Medicine Reports, vol. 9, no. 4, pp. 1395-1399
Publication Year
2014
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.
Keyword
Endoplasmic reticulum chaperonesEndoplasmic reticulum stressNaloxone
ISSN
1791-2997
Publisher
Spandidos Publ Ltd
DOI
http://dx.doi.org/10.3892/mmr.2014.1935
Type
Article
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > 1. Journal Articles
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