Figure 2.

BMT of PTE-treated diabetic HSCs protects against diabetes-induced epigenetic modifications on the ERβ promoter in PBMCs. Experimental rats were randomly separated into 4 groups as follows: rats with BMT of HSCs from CTL/VEH (BMT-CTL/VEH); rats with BMT of HSCs from STZ/VEH (BMT-STZ/VEH); rats with BMT of HSCs from STZ/RSV (BMT-STZ/RSV); and rats with BMT of HSCs from STZ/PTE (BMT-STZ/PTE). The rats were subjected to a model of cutaneous burn injury and PBMCs were collected for biomedical analysis after a 3-week period post-burn. (a) mRNA levels by qPCR, n = 4. (b) Protein quantitation by WB for (c), n = 5. (c) Representative picture for western blots. (d) ChIP analysis on ERβ promoter, n = 4. For bars in graphs marked with an asterisk, p < 0.05 vs BMT-CTL/VEH group. Data are expressed as mean ± SEM. BMT bone marrow transplantation, PTE pterostilbene, HSCs hematopoietic stem cells, ERβ estrogen receptor β, PBMCs peripheral blood mononuclear cells, CTL control, VEH vehicle, STZ streptozotocin, RSV resveratrol, NRF1 nuclear respiratory factor-1, SOD2 superoxide dismutase 2, H3K9me2 histone H3 lysine 9 dimethylation, H3K9me3 histone H3 lysine 9 trimethylation, H3K27me2 H3 lysine 27 dimethylation, H3K27me3 H3 lysine 27 trimethylation