The lncRNA ENST00000608794 acts as a competing endogenous RNA to regulate PDK4 expression by sponging miR-15b-5p in dexamethasone induced steatosis |
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| Affiliation: | 1. Group of Lipids and Cardiovascular Pathology, Biomedical Research Institute Sant Pau (IIB Sant Pau), Barcelona, Spain;2. CIBERCV, Instituto de Salud Carlos III, Madrid, Spain;3. Lipid Unit and Molecular Research Laboratory, IIS Aragón, Hospital Universitario Miguel Servet, Universidad de Zaragoza, Zaragoza, Spain;4. SISA Center for the Study of Atherosclerosis, Bassini Hospital, Cinisello B, Italy;5. IRCCS Multimedica, Milan, Italy;6. Cardiac Imaging Unit, Cardiology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain;7. Catalan Institute of Cardiovascular Sciences, Biomedical Research Institute Sant Pau (IIB Sant Pau), Barcelona, Spain;8. Department of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy;9. School of Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Perth, Western Australia, Australia;10. Institute of Biomedical Research of Barcelona (IIBB) - Spanish National Research Council (CSIC), Barcelona, Spain;1. Department of Cardiology, Shanghai General Hospital, School of Medicine, Shanghai Jiaotong University, Hongkou District, Shanghai, China;2. Department of Cardiology, Shanghai Institute of Cardiovascular Disease, Zhongshan Hospital, Fudan University, Shanghai 200080, China |
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| Abstract: | The contribution of ncRNAs, especially long non-coding RNAs (lncRNAs) to drug induced steatosis remains largely unknown. The aim of this study was to investigate the role of lncRNA ENST00000608794 in dexamethasone induced steatosis. We found that ENST00000608794 is expressed at higher levels in dexamethasone treated HepG2 cell, and ENST00000608794 can bind and be regulated by miR-15b-5p. Ectopic expression of ENST00000608794 enhanced steatosis and the protein expression of PDK4 which is a critical gene in lipid metabolism and also is a target of miR-15b-5p. However, the differentiated PDK4 expression between control and ectopic expression of ENST00000608794 was absence in the presence of miR-15b-5p inhibitor. Moreover, in dexamethasone treated HepG2 cell lines, ENST00000608794 increased whether with miR-15b-5p inhibitor treatment or not, while increase of PDK4 expression by dexamethasone was greatly compromised in the presence of miR-15b-5p mimic. Meanwhile, dexamethasone induced steatosis could be ameliorated by silencing ENST00000608794 or expressing miR-15b-5p. Taken together, the results suggested that ENST00000608794 plays an important role in dexamethasone induced steatosis, which was partly mediated by derepressing of PDK4 through competitively binding to miR-15b-5p. |
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