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Rottlerin induces cyclooxygenase-2 upregulation through an ATF4 and reactive oxygen species-independent pathway in HEI-OC1 cells

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Affiliated Author(s)
김동은박순형남성일권택규
Alternative Author(s)
Kim, Dong EunPark, Soon HyungNam, Sung IlKwon, Taeg Kyu
Journal Title
Molecular Medicine Reports
ISSN
1791-2997
Issued Date
2016
Keyword
rottlerincyclooxygenase‑2activating transcription factor 4p38 mitogen‑activated protein kinaseHEI‑OC1 cells
Abstract
Hearing loss can be caused by infection, inflammation, loud noise and ototoxic drugs. The induction of cyclooxygenase-2 (COX‑2) expression is an important event during the cellular inflammatory response. The present study investigated the effect of rottlerin on CO-2 mRNA and protein expression in HEI-OC1 cells. Cell viability was determined using an MTT assay. Western blotting was used to examine the expression of COX‑2, endoplasmic reticulum stress-associated transcription factors and activation of the MAPK pathway. ROS was measured using the fluorescent probe 2', 7'-dichlorodihydrofluorescein diacetate. Treatment with the natural protein kinase C δ inhibitor, rottlerin, was shown to increase COX‑2 expression at the protein and mRNA levels in a dose‑dependent manner. Rottlerin was shown to induce increased reactive oxygen species (ROS) generation, however, ROS were not critical for rottlerin‑induced upregulation of COX‑2 expression in HEI‑OC1 cells. In addition, rottlerin was shown to increase the phosphorylation of p38 mitogen-activated protein kinase (MAPK). The pharmacological inhibition of p38MAPK and suppression of activating transcription factor 4 (an ER stress‑associated transcription factor) expression by small interfering RNA inhibited rottlerin-induced COX‑2 upregulation. Furthermore, COX‑2 expression levels were increased further when cells were treated with rottlerin and interleukin‑1β or protein kinase C activator, PMA. In conclusion, the results of the present study demonstrated that rottlerin is a novel inducer of COX‑2 expression and identified the mechanisms involved in this process. Rottlerin may be considered a potential activator of repair and remodeling.
Department
Dept. of Otorhinolaryngology (이비인후과학)
Dept. of Immunology (면역학)
Publisher
School of Medicine
Citation
Seon Min Woo et al. (2016). Rottlerin induces cyclooxygenase-2 upregulation through an ATF4 and reactive oxygen species-independent pathway in HEI-OC1 cells. Molecular Medicine Reports, 14(1), 845–850. doi: 10.3892/mmr.2016.5320
Type
Article
ISSN
1791-2997
DOI
10.3892/mmr.2016.5320
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/32825
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
1. School of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학)
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