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. 2021 Feb 9;15:634781. doi: 10.3389/fnins.2021.634781

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Copyright © 2021 Liu, Liang, Jiang, Xu, Sun, Wang, Lin, Niu, Song, Zhang, Xue, Lu and Yao.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Hyperglycemia induces OXTR suppression through epigenetic modification and the subsequent dissociation of ERβ from the OXTR promoter. (A) The conditional immortalized ACS-5003 neurons were transiently transfected with either OXTR full length (pOXTR-2000) or deletion reporter plasmids. After 24 h, the cells were treated with either 5 mM low glucose (LG) or 25 mM high glucose (HG) for 3 days and the OXTR reporter activities were calculated, n = 5. ^∗P < 0.05, vs. pOXTR-2000 group. (B) The schematic picture for the potential transcriptional binding motif in the range of –900∼1100 (from transcription start site) on the OXTR promoter with two potential ERE binding sites marked in red as well as related mutation sites marked in green. (C) The cells were transiently transfected by either a wild type OXTR reporter construct (pOXTR-2000) or single point mutation at the site shown in panel (B), and then treated with either LG or HG for 3 days, and the OXTR reporter activities were calculated, n = 5. ^∗P < 0.05, vs. pOXTR-2000 group. (D) The cells were transiently transfected by OXTR full length (pOXTR-2000), single mutant, or double mutations as indicated, or infected by SOD2 lentivirus (↑SOD2), and then treated with either LG or HG for 3 days; the OXTR reporter activities were then calculated, n = 5. ^∗P < 0.05, vs. pOXTR-2000/LG group; ^¶ P < 0.05, vs. M-1005/ERE/LG group. (E,F) Cells were treated by either 4-day LG plus 4-day LG [LG(4d) + LG(4d)], or 4-day HG plus 4-day LG [HG(4d) + LG(4d)], or the cells were infected on day 4 by SOD2 lentivirus [HG(4d) + LG(4d)/↑SOD2]; the cells were then used for ChIP analysis: (E) ChIP analysis by potential transcription factors on OXTR promoter, n = 4; (F) ChIP analysis by potential histone methylation, n = 4. ^∗P < 0.05, vs. LG(4d) + LG(4d)/CTL group. (G–I) Cells were treated by either LG(4d) + LG(4d)/CTL or HG(4d) + LG(4d)/CTL, or the cells were infected on day 4 by either ERβ expression lentivirus [HG(4d) + LG(4d)/↑ERβ] or ERβ lentivirus knockdown [LG(4d) + LG(4d)/shERβ]; the cells were then harvested for biomedical analysis: (G) mRNA analysis, n = 4. (H) Protein quantitation, n = 5. (I) Representative western blotting pictures for (H). ^∗P < 0.05, vs. LG(4d) + LG(4d)/CTL group. Data were expressed as mean ± SEM.