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. 2009 Oct 12;25(4):769–781. doi: 10.1359/jbmr.091017

Fig. 1.

Fig. 1

E2 effects on osteoblast apoptosis, ROS levels, GSR activity, and p66shc phosphorylation are preserved in ERαNERKI/− mice. (A) Caspase-3 activity in calvaria cells isolated from wild-type (WT) control or ERαNERKI/− mice pretreated with vehicle (veh) or E2 (10−8 M) for 1 hour. Cells then were treated with veh, etoposide (5 × 10−5 M), or H2O2 (5 × 10−5 M) for 6 hours. (B) Osteoblast apoptosis determined by in situ end labeling in sections of undecalcified vertebral bone (L1–5) of 5-month-old WT or ERαNERKI/− mice sham operated or OVX. OVX animals received veh or E2 replacement for 6 weeks (n = 4 to 6 animal/group). (C) ROS levels and (D) GSR activity in bone marrow cells from 5-month-old WT, ERα+/−, ERαNERKI/+, and ERαNERKI/− mice sham operated or OVX and treated as described in B (n = 4 animals/group). (E) Phosphorylation of p66shc determined by Western blot analyses in vertebral lysates from the same mice as in C; each lane represents one animal. †p < .05 versus respective vehicle; *p < .05 versus OVX.