lncRNA AK054386 Functions as a ceRNA to Sequester miR-199 and Induce Sustained Endoplasmic Reticulum Stress in Hepatic Reperfusion Injury

Figure 2

The decrease in miR-199 is mediated by increased AK054386 in hepatic IRI. (a, b) The expression levels of the mature and premature forms of miR-199 were tested by qRT-PCR in both the (a) cell and (b) mouse hepatic IRI models. The values were normalized to U6. Student’s -test, . (c) Hierarchical clustering analysis of microarray data mined from the GEO database (GSE47412). (d) Putative binding sites for miR-199a-5p on AK054386 predicted with Miranda software. (e) The relative levels of AK054386 and miR-199 in mouse liver tissue from the control, ischemia, and IRI groups. RNA levels were quantified by qRT-PCR and normalized to GAPDH or U6. Five mice were analyzed in each group. ANOVA, . (f, g) Relative levels of the (f) mature and (g) premature forms of miR-199 in BNL-CL2 cells transfected with the AK054386 overexpression plasmid or knockdown siRNAs tested using qRT-PCR analysis. Data are shown as the of 6 independent experiments. ANOVA, and . (h) The expression levels of related factors in BNL-CL2 cells as measured by qRT-PCR analysis. GAPDH or U6 was used as the endogenous control. Data are shown as the of three independent experiments. Student’s -test, and .

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