Bioinformatics facilitating the use of microarrays to delineate potential miRNA biomarkers in aristolochic acid nephropathy
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Yana Lv1,*, Yumei Que3,*, Qiao Su2,3,*, Qiang Li2,3,*, Xi Chen1, Haitao Lu2,4
1Key Laboratory of Dai and Southern Medicine of Xishuangbanna Dai Autonomous Prefecture, Yunnan Branch, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences, Peking Union Medical College, Jinghong 666100, P.R. China
2Shanghai Center for Systems Biomedicine, Key Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, P.R. China
3Innovative Drug Research Centre and School of Chemistry and Chemical Engineering, Chongqing University, Chongqing 401331, P.R. China
4Tissue Repair and Regeneration Program, Institute of Health and Biomedical Innovation, School of Biomedical Sciences, Faculty of Health, Queensland University of Technology, Brisbane 4059, Australia
*These authors have contributed equally to this work
Xi Chen, email: [email protected]
Haitao Lu, email: [email protected]
Keywords: aristolochic acid nephropathy, microRNAs, network biology, functional analysis, biomarkers
Received: March 09, 2016 Accepted: June 30, 2016 Published: July 13, 2016
Aristolochic acid nephropathy (AAN) is a rapidly progressive acute or chronic tubulointerstitial nephritis (TIN). The present study attempted to explore the molecular mechanisms underlying the miRNA-directed development of AAN. Our differentially expressed analysis identified 11 DE-miRNAs and retrieved the target genes of these DE-miRNAs; then, network analysis and functional analysis further identified 6 DE-miRNAs (has-miR-192, has-miR-194, has-miR-542-3p, has-miR-450a, has-miR-584, has-miR-33a) as phenotypic biomarkers of AAN. Surprisingly, of has-miR-192 has been reported to be associated with the pathogenesis of AAN, and has-miR-194, has-miR-542-3p and has-miR-450a was first-time identified to link to the development of AAN. In addition, the expressional changes of has-miR-584 and has-miR-33a may be associated with the development of AAN as well, which must be further confirmed by the associated experiments. Taken together, our work reveals for the first time the regulatory mechanisms of miRNAs in the development of AAN and this will contribute to miRNA-based diagnosis and treatment of AAN.
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