Skip to main content
. 2015 Oct 8;65(1):149–163. doi: 10.2337/db15-0108

Figure 1.

Figure 1

High glucose in vivo and in vitro upregulates miR-200b expression through oxidative stress. A: miR-200b levels were determined by real-time PCR and normalized by U6 in WT and SOD1-overexpressing embryos from nondiabetic (ND) (nondiabetic dam glucose levels: 7.1 ± 0.3 mmol/L) and diabetic (DM) dams (diabetic dam glucose levels: 22.7 ± 1.2 mmol/L) and in WT embryos from diabetic dams with insulin pellet implantation throughout the experimental course (glucose levels in diabetic dam with insulin treatment: 13.6 ± 0.6 mmol/L). Experiments were conducted using 6 embryos from 6 different dams (n = 6) per group. *Significant differences (P < 0.05) compared with other groups. B: miR-200b levels in neural stem cells cultured under normal glucose (5 mmol/L glucose) or high glucose (16.6, 25, and 33.3 mmol/L glucose) conditions for 24 h. C: miR-200b levels in cells cultured under 5 mmol/L or 25 mmol/L glucose conditions for 12, 24, and 48 h. D: miR-200b levels in cells under 5 mmol/L or 25 mmol/L glucose in the absence or presence of the SOD1 mimetic tempol (100 μmol/L) for 24 h. E: miR-200b levels in cells cultured under 5 mmol/L glucose conditions with or without high mannitol (11.7, 20, and 28.3 mmol/L mannitol) for 24 h. F: miR-200b levels in cells cultured under 5 mmol/L glucose conditions with or without 20 mmol/L mannitol for 12, 24, and 48 h. Cell culture experiments were repeated three times (n = 3). *Significant differences (P < 0.05) compared with other groups (A, B, and D) or the 5 mmol/L glucose groups (C).