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Fig. 2. MiR-21 suppresses PARP-1 expression and PARP-1 is a direct target of miR-21. (A–C) The 16HBE cells were transfected with NC, miR-21 mimics, miR-21 inhibitor, miR-21 mimics + PARP-1 plasmid, or miR-21 inhibitor + PARP-1 siRNA. Expressions of miR-21 and PARP-1 mRNA were detected by qRT-PCR and the protein expression of PARP-1 was detected by Western blot 48 h post-transfection. The experiments were replicated three times and presented as mean ± SD. *p < 0.05 vs. NC group, **p < 0.01 vs. NC group, p < 0.05 vs. miR21 or miR-21 inhibitor group, ††p < 0.01 vs. miR-21 inhibitor group. (D) The potential binding site between miR-21 and 3’UTR of PARP-1 mRNA is shown. Luciferase activities of 16HBE cells transfected with NC, miR-21 mimics, PARP-1 Wt, PARP-1 Mut, miR-21 mimics + PARP-1 Wt, or miR-21 mimics + PARP-1 Mut were measured by luciferase reporter assay. The experiments were replicated three times and presented as mean ± SD. **p < 0.01 vs. NC group. (E) Western blot was used to detect the binding capacity of biotin-labeled miR-21 mimics probes with PARP-1 protein. The experiments were replicated three times. miR-21, microRNA-21; PARP-1, poly (ADP-ribose) polymerase-1; 16HBE, Human bronchial epithelial cell; NC, normal control; siRNA, small interfering RNA; siPARP-1, PARP-1 siRNA; UTR, untranslated region; Wt, wild type; Mut, mutant.
Korean J Physiol Pharmacol 2022;26:239-253 https://doi.org/10.4196/kjpp.2022.26.4.239
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