LI Huiting1, SUN Fei2, YUAN Ping1, GONG Sugang1, HE Jing1, WANG Lan1*, LIU Jinming1*,SUN Fei,YUAN Ping,et al.Regulatory mechanism of miR-1290 in non-alcoholic fatty liver disease[J].Journal of Tongji University(Medical Science),2024,45(5):641-648. [点击复制]
Regulatory mechanism of miR-1290 in non-alcoholic fatty liver disease
LI Huiting1, SUN Fei2, YUAN Ping1, GONG Sugang1, HE Jing1, WANG Lan1*, LIU Jinming1*,SUN Fei,YUAN Ping,GONG Sugang,HE Jing,WANG Lan,LIU Jinming
(Department of Respiratory Medicine, Affiliated Hospital of Nantong University, Nantong 226000, Jiangsu Province, China;Department of Endocrinology, Shanghai Pudong New Area Gongli Hospital, Shanghai 200135, China;Department of Cardio-Pulmonary Circulation, Shanghai Pulmonary Hospital, School of Medicine, Tongji University, Shanghai 200092, China)
Abstract:
Objective To explore the role and potential regulatory mechanism of miR-1290 in non-alcoholic fatty liver disease(NAFLD).
Methods GenBank GEO database,Targetscan, mirBase, miRanda biological databases were screened to find out miRNAs abnormally expressions in NAFLD, and GO and KEGG analysis target gene prediction databases were used to select miRNAs related to GH-IGF1 axis. NAFLD was induced in HL-7702(L02) cells to establish L02 NAFLD cell line. L02 cells(control group) and NAFLD cells were treated with 25, 250 ng/mL rhGH and 50, 500 ng/mL rhIGF1, respectively; and the expression of miRNAs was detected with RT-qPCR and verified by cell transfection.
Results In NAFLD group, the expressions of miR-1290, miR-16, miR-122 were significantly higher than those in control(P<0.05); after treatment of rhGH and rhIGF1 the expression levels in NAFLD group were decreased, compared to those in control group(P<0.05). In L02 NAFLD cells transfected with mimics miR-1290, the expression levels of GHR, IGFBP3, FASN mRNA were significantly higher than those in control group(P<0.05).
Conclusion MiRNAs are abnormally expressed in NAFLD, miR-1290 has higher expression in NAFLD cells, which may act on lipid metabolism and insulin resistance in NAFLD through GH/IGF1 axis.
