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. 2018 Sep 7;14(11):1545–1557. doi: 10.7150/ijbs.24032

Figure 4.

Figure 4

PTEN is a direct target of miR-188-5p and triptolide can promote PTEN expression. (A) Quantification of miR-188-5p gene expression in the HK-2 cells (n=4). (B) Quantification of miR-188-5p gene expression in rat kidneys (n=15). (C) miR-188-5p sequence and its potential binding sites in the wild-type PTEN-3ʹ-UTR. The complementary binding site was replaced in the mutant PTEN 3ʹ-UTR. (D) Dual-luciferase reporter assay with wild-type PTEN-3ʹ-UTR and mutated PTEN- 3ʹ-UTR reporter gene in 293T cells transfected with miR-188-5p mimic or miR-mNC for 24 h (n=4). (E) Quantification of PTEN gene expression in the HK-2 cells (n=4). Data are expressed as the mean ± SD. **P < 0.01 vs. the miR-mNC group. *P < 0.05 vs. the NG group. # P < 0.05 vs. the HG group. NC: normal control; DKD: diabetic kidney disease; TP: triptolide; NG: normal glucose; MA: mannitol; HG: high glucose; miR-188-5pm: miR-188-5p mimic; miR-mNC: negative control of miR-188-5p mimic.