miR-222 targets ACOX1, promotes triglyceride accumulation in hepatocytes
miR-222 targets ACOX1, promotes triglyceride accumulation in hepatocytes作者机构:Department of Digestive Diseases Huashan Hospital Fudan University
出 版 物:《Hepatobiliary & Pancreatic Diseases International》 (国际肝胆胰疾病杂志(英文版))
年 卷 期:2019年第18卷第4期
页 面:360-365页
核心收录:
学科分类:1002[医学-临床医学] 100201[医学-内科学(含:心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
基 金:supported by grants from the National Natu-ral Science Foundation of China(81420108005 and 81630016) the Natural Science Foundation and Major Basic Research Program of Shanghai(16JC1420104) the Ministry of Science and Technol-ogy of China(2013CB945401)
主 题:ACOX1 Hepatocyte steatosis miR-222 NAFLD β-hydroxybutyrate
摘 要:Background:Non-alcoholic fatty liver disease(NAFLD)is one of the most prevalent chronic liver ***,the exact pathogenesis of NAFLD remains to be *** the association with tumors and cardiovascular diseases,the role of miR-222 in NAFLD remains *** present study was to investigate the role of miR-222 in ***:Wild-type C57BL/6 mice were fed a high-fat diet for 12 weeks to induce *** human liver cell line(L02)was cultured with free fatty acid(FFA)-containing medium to stimulate cell *** mRNA levels of miR-222 and acyl Coenzyme A xidase 1(ACOX1)were detected by quantitative-PCR(Q-PCR).The prediction of ACOX1 as the target gene for miR-222 was conducted via *** overexpression or inhibition of miR-222 was mediated by miR-222 mimics or antagomir,and intracellular triglyceride levels were measured using a triglyceride *** reporter assays verified ACOX1 as the target gene for ***:miR-222 was significantly elevated in both the in vivo and in vitro NAFLD *** of miR-222 significantly increased triglyceride content in the L02 cells,while inhibition of miR-222 expression restricted the accumulation of *** of miR-222 significantly inhibited ACOX1 *** transfection assays verified that ACOX1 3-UTR luciferase reporter activity could be inhibited by miR-222 ***:The present study suggested that miR-222 promotes the accumulation of triglycerides by inhibiting ACOX1.