Skip to main content
. Author manuscript; available in PMC: 2016 Jan 28.
Published in final edited form as: Calcif Tissue Int. 2015 Feb 25;96(5):465–475. doi: 10.1007/s00223-015-9967-7

Fig. 4.

Fig. 4

Loss of LNX2 accelerates pre-osteoclast apoptosis. (A) BMMs were cultured with M-CSF alone (BMM) or M-CSF and RANKL (pOC) for two days. Cell proliferation rate was measured by BrdU incorporation ELISA. *** p < 0.001 vs BMM by one-way ANOVA. (B) and (C) BMMs were cultured with M-CSF and RANKL for two days to generate pre-osteoclasts. The cells were then either untreated (oh) or were serum and cytokine starved for 3 hours (3h). Apoptosis was assessed by (B) Cell Death Detection ELISA PLUS kit, which detects cytoplasmic histone-associated DNA fragmentation and (C) western blots using antibodies against cleaved Caspase-3 and PARP. Actin served as a loading control. Data in (A) and (B) were presented as mean ± S.D, n = 6, * p < 0.05, *** p <0.001 vs LUC-sh by one-way ANOVA. The experiments were repeated twice.