[miR-494 promotes islet β cell proliferation, inhibits apoptosis and increases insulin secretion by activating Wnt/β-catenin signaling pathway].

Objective To investigate the relation between the miR-494 expression with pancreatic islets β cell function and gestational diabetes mellitus. Methods Twenty patients with gestational diabetes mellitus and healthy subjects were enrolled. The content of miR-494 in peripheral blood was measured by reverse transcription PCR. INS-1 cells were cultured and treated with low glucose (3.3 mmol/L) and high glucose (16.7 mmol/L), respectively. The insulin concentration was tested by ELISA to evaluate the insulin secretion of islet cells stimulated by high glucose. Cells were collected, after treated with miR-494 mimics control, miR-494 mimics, miR-494 inhibitor control and miR-494 inhibitor for 24 hours, 48 hours and 72 hours, respectively. The activity of INS-1 cells was detected by MTT assay; Apoptosis was detected by flow cytometry. Reverse transcription PCR and Western blot analysis were used to detect the mRNA and protein expression of Wnt3a, β-catenin, cyclin D1 and c-Myc, respectively. Results Compared with the normal control, fasting insulin, fasting blood glucose, 1 hour-blood glucose and 2 hour-blood glucose in patients with gestational diabetes mellitus increased significantly. The content of miR-494 in peripheral blood decreased. The insulin concentration in the supernatant of INS-1 cells overexpressing miR-494 increased. When high glucose was given, the overexpression of miR-494 further promoted insulin secretion. Overexpression of miR-494 significantly promoted INS-1 cell activity and inhibited INS-1 cell apoptosis. miR-494 significantly promoted the protein expression of Wnt3a, β-catenin, cyclin D1 and c-Myc. miR-494 inhibitor treatment showed the opposite results. Conclusion miR-494 promotes islet β cell proliferation, inhibits apoptosis and increases insulin secretion by activating Wnt/β-catenin signaling pathway.