Chen Qiuchi, Fang Wei, Shen Yanan, Xu Dan, Chen Qiang, Cui Kun, Mai Kangsen, Ai Qinghui
Key Laboratory of Aquaculture Nutrition and Feed, Ministry of Agriculture and Rural Affairs, and Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, 5 Yushan Road, Qingdao, Shandong, 266003, PR China.
Key Laboratory of Aquaculture Nutrition and Feed, Ministry of Agriculture and Rural Affairs, and Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, 5 Yushan Road, Qingdao, Shandong, 266003, PR China; Laboratory for Marine Fisheries Science and Food Production Processes, Qingdao National Laboratory for Marine Science and Technology, 1 Wenhai Road, Qingdao, Shandong, 266237, PR China.
Free Radic Biol Med. 2022 May 20;185:67-75. doi: 10.1016/j.freeradbiomed.2022.04.009. Epub 2022 Apr 27.
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.
先前的研究表明，内质网（ER）应激以多种方式导致炎症。然而，细胞死亡诱导DFF45样效应因子b（Cideb），一种在肝脏脂质代谢中起重要作用的脂滴（LD）相关蛋白，是否参与这一过程尚未见报道。在本研究中，我们证明单独的cideb缺陷不会引发肝脏中的剧烈炎症。然而，在ER应激下，Chop（C/EBP同源蛋白）抑制了cideb的表达，这抑制了肝脏中脂蛋白的转运，导致肝脂肪变性和氧化应激加剧，最终加剧了炎症。我们的结果可能提供了一种新的机制来解释ER应激引发的炎症。
