Figure 4: Impaired APEX1 contributes to DNMT1 upregulation and DNA hypermethylation induced by high glucose treatment in dental epithelial stem cells (DESCs). | Scientific Reports

Figure 4: Impaired APEX1 contributes to DNMT1 upregulation and DNA hypermethylation induced by high glucose treatment in dental epithelial stem cells (DESCs).

From: Maternal diabetes modulates dental epithelial stem cells proliferation and self-renewal in offspring through apurinic/apyrimidinicendonuclease 1-mediated DNA methylation

Figure 4

(A) Western blot analysis of DNMT1 and DNMT3a levels in the cervical loops of offspring from control and diabetic dams; *P < 0.05 vs. control. (B) Global DNA methylation levels in the cervical loop of offspring from control and diabetic dams; *P < 0.05 vs. control. (C) DESCs treated with high glucose showed significant upregulation of DNMT1 and overexpression of APEX1WT, whereas redox-deficient APEX1C65A attenuated the DNMT1 upregulation induced by high-glucose treatment; *P < 0.05 vs. control; #P < 0.05 vs. high glucose. (D) High glucose treatment induced a significant increase in global DNA methylation levels and overexpression of APEX1WT, whereas redox-deficient APEX1C65A attenuated global DNA hypermethylation induced by high glucose treatment; *P < 0.05 vs. control; #P < 0.05 vs. high glucose. (E) Western blotting showed that Apex1 knockdown or inhibition of redox activity by the inhibitor E3330 enhanced DNMT1 expression, but did not affect DNMT3a expression; *P < 0.05 vs. control. (F) Apex1 knockdown or inhibition of redox activity by the inhibitor E3330 significantly increased global DNA methylation levels; *P < 0.05 vs. control.

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