tailieunhanh - Báo cáo khoa học: The rno-miR-34 family is upregulated and targets ACSL1 in dimethylnitrosamine-induced hepatic fibrosis in rats

The mechanisms whereby hepatic fibrosis develops in chronic liver diseases remain incompletely defined. Here, we sought to examine whether micro-RNA (miRNA) became dysregulated in dimethylnitrosamine-induced hepatic fibrosis in rats. Our microarray analysis revealed that the miR-34 family was upregulated along with other miRNAs in liver fibrotic tissues. Six miRNAs, such as rno-miR-878, were downregulated. | 1FEBS Journal The rno-miR-34 family is upregulated and targets ACSL1 in dimethylnitrosamine-induced hepatic fibrosis in rats Wei-Qing Li1 Chao Chen2 Mi-Die Xu1 Jia Guo3 Yi-Ming Li4 Qing-Mei Xia5 Hui-Min Liu1 Jin He1 Hong-Yu Yu1 and Liang Zhu2 1 Department of Pathology Changzheng Hospital Second Military MedicalUniversity Shanghai China 2 Department of Gastroenterology Changzheng Hospital Second Military MedicalUniversity Shanghai China 3 Department of Ultrasonography Eastern Hepatobiliary Surgery Hospital Second Military MedicalUniversity Shanghai China 4 Department of Neurosurgery Changzheng Hospital Second Military MedicalUniversity Shanghai China 5 Shanghai SunBio MedicalBiotechnology Co. Ltd China Keywords acyl-CoA synthetase long-chain family member 1 ACSL1 gene ontology hepatic fibrosis miR-34a miR-34c rat Correspondence L. Zhu Department of Gastroenterology Changzheng Hospital Second Military MedicalUniversity 415 Fengyang Road Shanghai 200003 China Fax 86 21 63520020 Tel 86 21 81885261 E-mail czzhuliang@ . Yu Department of Pathology Changzheng Hospital Second Military MedicalUniversity 415 Fengyang Road Shanghai 200003 China Fax 86 21 63520020 Tel 86 21 81886122 E-mail yuhongyu795@ The mechanisms whereby hepatic fibrosis develops in chronic liver diseases remain incompletely defined. Here we sought to examine whether micro-RNA miRNA became dysregulated in dimethylnitrosamine-induced hepatic fibrosis in rats. Our microarray analysis revealed that the miR-34 family was upregulated along with other miRNAs in liver fibrotic tissues. Six miRNAs such as rno-miR-878 were downregulated. The findings were confirmed by RT-PCR assays. Gene ontology analysis further showed that many of these dysregulated miRNAs were involved in lipid fatty acid metabolism. The acyl-CoA synthetase long-chain family member 1 ACSL1 gene contained specific binding sites for miR-34a miR-34c. Additional enhanced green fluorescence protein reporter activity assays .

TÀI LIỆU LIÊN QUAN