Fig. 3

HAT activation mediates GEE-potentiated histone acetylation and BDNF expression in AD offspring. (a,b) GEE increases acetylation of histone 4 (H4ac) and histone 3 (H3ac) without changing the total levels of H4 and H3 in the embryo (E19), as measured by western blotting (n = 3, unpaired t-test). (d,e) GEE increases H4 acetylation at K12 (H4K12ac) and H3 at K14 (H3K14ac) in 7-m-old offspring hippocampus without changing the total levels of H4 and H3 (n = 3, unpaired t-test). (c,f) GEE activates histone acetyltransferase (HAT) without changing histone deacetylases (HDACs) in embryos (Ctrl, n = 6, GEE, n = 8, unpaired t-test) and 7-m-old offspring hippocampus (n = 9 per group, unpaired t-test). (g-i) Simultaneous inhibition of HAT by intraperitoneal injection of C646 during pregnancy abolishes GEE-induced H4 and H3 acetylation and as well as BDNF upregulation (n = 4~6, one–way ANOVA). Data are presented as the mean ± s.e.m. of at least 3 independent litters of mice. *P < 0.05, **P < 0.01 vs. Ctrl; ^#P < 0.05, ^##P < 0.01 vs. GEE