Research Paper Volume 16, Issue 7 pp 5916—5928

Figure 4. miRNA-199a-5p attenuates 5-FU induced toxicity in cardiomyocytes by targeting ATF 6. (A) The bioinformatics analysis indicates the binding sites between ATF6 and miRNA-199a-5p; (B) the dual luciferase reporter assay was used to verify the binding between miRNA-199a-5p and ATF6. The miRNA-199a-5p mimic decreased the luciferase activity of cells transfected with vector containing wild-type ATF6 sequence; (C) the cardiomyocytes cells were pretreated with miRNA-199a-5p, and the protein expression of ATF6, GRP78, CHOP and PERK decreased in 5-FU stimulated cells; (D–G) the adenoviral vector encoding full-length of ATF6 (Ad-ATF6) was introduced to cardio myocyte cells. The increasing expression of ATF6 decreased cell viability, SOD activity, GSH/GSSG ratio and alternatively increased LDH level in cardiomyocyte.