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The rno‐miR‐34 family is upregulated and targets ACSL1 in dimethylnitrosamine‐induced hepatic fibrosis in rats
Author(s) -
Li WeiQing,
Chen Chao,
Xu MiDie,
Guo Jia,
Li YiMing,
Xia QingMei,
Liu HuiMin,
He Jin,
Yu HongYu,
Zhu Liang
Publication year - 2011
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2011.08075.x
Subject(s) - microrna , downregulation and upregulation , hepatic fibrosis , fibrosis , biology , microarray analysis techniques , gene , microarray , real time polymerase chain reaction , cancer research , reporter gene , microbiology and biotechnology , gene expression , medicine , genetics
The mechanisms whereby hepatic fibrosis develops in chronic liver diseases remain incompletely defined. Here, we sought to examine whether microRNA (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 indicated that the miR‐34 family targeted ACSL1 . Our RT‐PCR and immunoblotting assays further demonstrated that both the mRNA and protein levels of ACSL1 were markedly reduced in fibrotic liver tissues. Our findings suggest that miRNA becomes dysregulated during hepatic fibrosis, and that the miR‐34 family may be involved in the process by targeting ACSL1 .