Figure 4 | Cell Death & Disease

Figure 4

From: lncRNA MIAT functions as a competing endogenous RNA to upregulate DAPK2 by sponging miR-22-3p in diabetic cardiomyopathy

Figure 4

MIAT is targeted by miR-22-3p in an AGO2-dependent manner. (a) Bioinformatics prediction using miRcode indicated that MIAT sequence contained the putative binding site of miR-22-3p. (b) The miR-22-3p expression was increased in HEK293 cells transfected with miR-22-3p mimic. (c) The cDNA of MIAT was cloned into the downstream of luciferase gene (Luc-MIAT-Wt) and transfected into HEK293 cells with miR-22-3p mimic or control oligonucleotide. To avoid unspecific binding, the miR-22-3p binding sites in MIAT were mutated to generate Luc-MIAT-Mut. Luciferase activity was detected 48 h after transfection. (d) The AGO2 expression was detected in cardiomyocytes under basic conditions and high glucose exposure. (e) The RIP assay was performed to confirm whether MIAT and miR-22-3p could directly bind to AGO2 in cardiomyocytes. (f) The RIP experiments were conducted under basic conditions and high glucose exposure, and then the MIAT levels were determined. *P<0.05 (n=3 independent experiments)

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