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Brief Report

Comparison of epigenetic profiles of human oral epithelial cells from HIV-positive (on HAART) and HIV-negative subjects

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Pages 703-709 | Received 23 Jan 2013, Accepted 13 May 2013, Published online: 17 May 2013

Figures & data

Figure 1. (A) POEC growth comparison (HIV+O/H vs. Normal): Cell growth assays for POECs isolated from 3 HIV+O/H and three normal subjects were performed using PrestoBlue® Cell Viability Reagent. (*p < 0.05). (B) Comparison of HDAC1 protein levels in the nuclear extract of POECs isolated from 9 normal and 6 HIV+O/H subjects. (*p < 0.05, Mann–Whitney t test)

Figure 1. (A) POEC growth comparison (HIV+O/H vs. Normal): Cell growth assays for POECs isolated from 3 HIV+O/H and three normal subjects were performed using PrestoBlue® Cell Viability Reagent. (*p < 0.05). (B) Comparison of HDAC1 protein levels in the nuclear extract of POECs isolated from 9 normal and 6 HIV+O/H subjects. (*p < 0.05, Mann–Whitney t test)

Figure 2. Comparison of DNMT activity (A), DNMT1 (B), DNMT3A (C) and DNMT3B (D) protein levels in the nuclear extract of POECs isolated from 10 normal subjects vs. 9 HIV+O/H subjects. (E) Correlation between DNMT activity and the levels of three individual DNMTs.

Figure 2. Comparison of DNMT activity (A), DNMT1 (B), DNMT3A (C) and DNMT3B (D) protein levels in the nuclear extract of POECs isolated from 10 normal subjects vs. 9 HIV+O/H subjects. (E) Correlation between DNMT activity and the levels of three individual DNMTs.

Figure 3. Correlation between DNMT activity and global DNA methylation. Total global DNA methylation and DNMT activity in nuclear extract of eight subjects were measured. DNA methylation (expressed as 5-mC% in total DNA) and DNMT activity (expressed as OD/hr/mg) were plotted against each other for each of the subjects.

Figure 3. Correlation between DNMT activity and global DNA methylation. Total global DNA methylation and DNMT activity in nuclear extract of eight subjects were measured. DNA methylation (expressed as 5-mC% in total DNA) and DNMT activity (expressed as OD/hr/mg) were plotted against each other for each of the subjects.

Figure 4. POECs from 9 normal and 7 HIV+O/H subjects were grown to semi-confluence (80%) and treated with FnCW (10 μg/ml) for 18 h, respectively. The levels of hBD-2 in media supernatant of FnCW treated and untreated POECs from HIV+O/H and normal subjects were measured by ELISA. Mean (± SD) fold changes in FnCW induced hBD-2 release for the two cohorts, i.e., HIV+O/H and HIV- subjects, were compared (A). Mean (± SD) values of total (B) and phophorylated p38 (p-p38) (C) levels in the cytoplasmic extracts of POECs from the same two cohorts of subjects were measured and compared. The ratios of p-p38 to total p38 were also compared (D). (E) The correlation between the levels of pp38 and the induction of hBD-2 by FnCW.

Figure 4. POECs from 9 normal and 7 HIV+O/H subjects were grown to semi-confluence (80%) and treated with FnCW (10 μg/ml) for 18 h, respectively. The levels of hBD-2 in media supernatant of FnCW treated and untreated POECs from HIV+O/H and normal subjects were measured by ELISA. Mean (± SD) fold changes in FnCW induced hBD-2 release for the two cohorts, i.e., HIV+O/H and HIV- subjects, were compared (A). Mean (± SD) values of total (B) and phophorylated p38 (p-p38) (C) levels in the cytoplasmic extracts of POECs from the same two cohorts of subjects were measured and compared. The ratios of p-p38 to total p38 were also compared (D). (E) The correlation between the levels of pp38 and the induction of hBD-2 by FnCW.
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