RelA/p65 promotes osteoclast differentiation by blocking a RANKL-induced apoptotic JNK pathway in mice
J. Clin. Invest. Sergio Vaira, et al. 118:2088 doi:10.1172/JCI33392 [
Go to this article.]
Figure 1RelA is important for basal and stimulated OC formation in vivo. (
A) TRAP-stained sections of vertebrae from
Rela+/+ and
Rela–/– RCs 4 months after bone marrow reconstitution. Scale bar: 100 μm. (
B) Histomorphometric analysis was performed on TRAP-stained sections to determine the OC number (N.Oc./mm) and OC surface (Oc.S./BS.). *
P < 0.05;
n = 8/group. (
C)
Rela+/+ and
Rela–/– RCs were injected with 100-μg RANKL or PBS daily for 5 days and sacrificed on the sixth day. TRAP-stained coronal sections of calvaria at the sagittal suture show a consistent increase in OCs along sutures and sinusoids only in
Rela+/+ RANKL-treated animals. Scale bar: 200 μm. (
D) Quantification of the N.Oc./mm and Oc.S./BS. (percentage of bone surface covered by OCs) along calvarial surfaces of mice in
C confirms the significant difference in response of
Rela+/+ and
Rela–/– RCs to RANKL injection. In the PBS-injected animals, only rare OCs are detected in either genotype.
†P < 0.005;
n = 5/group. (
E) Serum levels of TRAP5b were determined 1 day prior to first RANKL injection (baseline) and at sacrifice on day 6 (RANKL).
‡P = 0.01;
n = 5/group.
