Suppression of cideb under endoplasmic reticulum stress exacerbated hepatic inflammation by inducing hepatic steatosis and oxidative stress

被引:6
|
作者
Chen, Qiuchi [1 ]
Fang, Wei [1 ]
Shen, Yanan [1 ]
Xu, Dan [1 ]
Chen, Qiang [1 ]
Cui, Kun [1 ]
Mai, Kangsen [1 ,2 ,3 ]
Ai, Qinghui [1 ,2 ,3 ]
机构
[1] Minist Agr & Rural Affairs, Minist Educ, Key Lab Aquaculture Nutr & Feed, Key Lab Mariculture, 5 Yushan Rd, Qingdao 266003, Shandong, Peoples R China
[2] Qingdao Natl Lab Marine Sci & Technol, Lab Marine Fisheries Sci & Food Prod Proc, 1 Wenhai Rd, Qingdao 266237, Shandong, Peoples R China
[3] Ocean Univ China Yushan Rd, Qingdao 266003, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
ER stress; Inflammation; Hepatic steatosis; Oxidative stress; Cideb; KAPPA-B; PROTEIN; ER; ACTIVATION; LIPOGENESIS; PATHWAY; INSULIN;
D O I
10.1016/j.freeradbiomed.2022.04.009
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Previous studies have shown that endoplasmic reticulum (ER) stress contributes to inflammation in several manners. However, whether cell death inducing DFF45-like effector b (Cideb), a lipid droplet (LD) associated protein that plays an important role in hepatic lipid metabolism, participates in this process has not been reported. In the present study, we demonstrated that deficiency of cideb alone did not trigger violent inflammation in the liver. However, the expression of cideb was suppressed by Chop (C/EBP homologous protein) under ER stress, which inhibited the transport of lipoproteins in the liver and led to the exacerbation of hepatic steatosis and oxidative stress, and ultimately exacerbated inflammation. Our results might provide a novel mechanism explaining inflammation triggered by ER stress.
引用
收藏
页码:67 / 75
页数:9
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