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Fig. 4 | Molecular Medicine

Fig. 4

From: Phosphorylation of BCL2 at the Ser70 site mediates RANKL-induced osteoclast precursor autophagy and osteoclastogenesis

Fig. 4

BCL2 mutation at S70 promoted OCP apoptosis while BCL2 mutation at S87 was contrary. A OCPs transfected with WT BCL2 or S70A BCL2 were treated with RANKL for the indicated times in α-MEM with 2.5% FBS. Cleaved caspase3 and cleaved PARP were detected using western blotting assays. B, C Dynamic changes in cleaved caspase3 and cleaved PARP in OCPs between the WT group and the S70A group. The protein expression level was normalized to that of the control samples (4 h in the WT group). D OCPs transfected with WT BCL2 or S87A BCL2 were treated with RANKL for the indicated times in α-MEM with 2.5% FBS. Cleaved caspase3 and cleaved PARP were detected using western blotting assays. E, F Dynamic changes in cleaved caspase3 and cleaved PARP in OCPs between the WT group and the S87A group. The protein expression level was normalized to that of the control samples (4 h in the WT group). B, C, E, F At different time points, pairwise comparisons were made between the WT group and the mutant group. G The transfected OCPs were treated with RANKL for 48 h in α-MEM with 2.5% FBS. Cell apoptosis was examined by flow cytometry of Annexin/PI staining. H The percentages of apoptotic cells (ANNEXIN-positive cells) are shown in the histograms according to the results in G. The experiments were replicated at least three times. Data are presented as the mean ± SEM from three independent experiments. ***P < 0.001, **P < 0.01, *P < 0.05

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