Acetylation of the Pro-Apoptotic Factor, p53 in the Hippocampus following Cerebral Ischemia and Modulation by Estrogen
Figure 5
The ability of estrogen to suppress the elevation of Acetyl p53-Lysine373 levels following GCI is lost in long-term estrogen deprived animals.
(A) Representative DAB images of immediate (Imm, 7 d) and 10 week (10 W) E2 deprived animals at 24 h following ischemic reperfusion. Note that 17β−E2 attenuation of Acetyl p53-Lysine373 levels is lost in long-term E2 deprived (10 W) animals and that there is robust p53 acetylation in all 10 W animals. Magnification 40X. (B) Semi-quantitative analysis of Acetyl p53-Lysine373-positively stained cells in Imm (7 d) and long-term (10 W) E2-deprived animals, expressed as folds vs. sham in 4–5 sections. *p<0.05 vs. Sham, #p<0.05 vs. Pla or 10 W E2 group; NS = No significant difference. n = 4–5 animals per treatment group.