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Melatonin ameliorates ER stress-mediated hepatic steatosis through miR-23a in the liver

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Author(s)
이재호박재형배재훈송대규임승순백원기
Alternative Author(s)
Lee, Jae HoPark, Jae HyungBae, Jae HoonSong, Dae KyuIm, Seung SoonBaek, Won Ki
Publication Year
2015
Abstract
The endoplasmic reticulum (ER) stress induces hepatic steatosis and inflammation in the liver. Although melatonin ameliorates ER stress-target genes, it remains unknown whether melatonin protects against hepatic steatosis as well as inflammation through regulation of miRNA. MicroRNAs have been identified as pivotal regulators in the field of gene regulation and their dysfunctions are a common feature in a variety of metabolic diseases. Especially, among miRNAs, miR-23a has been shown to regulate ER stress. Herein, we investigated the crucial roles of melatonin in hepatic steatosis and inflammation in vivo. Tunicamycin challenge caused increase of hepatic triglyceride and intracellular calcium levels through activation of ER stress, whereas these phenomena were partially disrupted by melatonin. We also demonstrated that expression of miR-23a stimulated with tunicamycin was rescued by melatonin treatment, resulting in reduced ER stress in primary hepatocytes. Overall, these results suggest a new function of melatonin that is involved in ameliorating ER stress-induced hepatic steatosis and inflammation by attenuating miR-23a. Melatonin may be useful as a pharmacological agent to protect against hepatic metabolic diseases due to its ability to regulate expression of miR-23a.

Keywords
Melatonin;
miR-23a;
ER stress;
Hepatic steatosis;
Calcium
Department
Dept. of Anatomy (해부학)
Dept. of Physiology (생리학)
Dept. of Microbiology (미생물학)
Publisher
School of Medicine
Citation
Biochemical and Biophysical Research Communications, Vol.458(3) : 462-469, 2015
Type
Article
ISSN
0006-291X
DOI
10.1016/j.bbrc.2015.01.117
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/35166
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