NUP85 alleviates lipid metabolism and inflammation by regulating PI3K/AKT signaling pathway in nonalcoholic fatty liver disease
Yincui Wu, Qi Yan, Si-qing Yue, Linxin Pan, Dashuai Yang, Liang-song Tao, Zeyuan Wei, Rong Fan, Qian Cheng, Meng-qi Han, Fucheng Zuo, Junfa Yang, Jiajia Xu, Zheng‐Rong Shi, Jian Du, Zhao-lin Chen, Tao Xu
Abstract
, AML-12 cells were stimulated with 2 mm free fatty acids (FFA) for 24 h. Results also proved that NUP85 significantly increased in model group, and increased lipid accumulation and inflammation level. Besides, NUP85 protein could interact with C-C motif chemokine receptor 2 (CCR2). Furthermore, when NUP85 protein expressed at an extremely low level, the expression level of CCR2 protein also decreased, accompanied with an inhibition of phosphorylation of phosphoinositol-3 kinase (PI3K)-protein kinase B (AKT) signaling pathway. What is more, trans isomer (ISRIB), a targeted inhibitor of NUP85, could alleviate NAFLD. In summary, our findings suggested that NUP85 functions as an important regulator in NAFLD through modulation of CCR2.