Figure 4. Bcl-xL regulates osteoclast survival.

(A) Adenovirus-mediated overexpression of Bcl-xL markedly suppressed cell death of wild-type osteoclasts. TRAP staining of representative cultures is also shown. (B) Western blotting of cleaved caspase-3 using β-actin as an internal control. Bcl-xL overexpression suppressed the amount of cleaved caspase-3 in osteoclasts. Lanes from this panel were run on the same gel but were noncontiguous. (C) Adenovirus vector–mediated overexpression of Cre recombinase efficiently downregulated Bcl-xL expression in osteoclasts differentiated from Bcl-x^fl/fl mouse bone marrow cells. (D) Increased cell death in Bcl-x cKO osteoclasts. TRAP staining of representative cultures is also shown. (E) Western blotting of cleaved caspase-3 using β-actin as an internal control. Bcl-x cKO osteoclasts exhibited the amount of increased cleaved caspase-3. (F) Decreased survival in Bcl-x cKO osteoclasts was rescued by Bcl-xL overexpression. Osteoclasts were generated from bone marrow cells of Bcl-x cKO mice or their normal Bcl-x^fl/fl littermates, infected with either AxGFP or AxBcl-xL, and subjected to survival assay. After 24 h of culture, osteoclasts derived from Bcl-x cKO mouse bone marrow cells exhibited reduced survival, which was rescued by Bcl-xL introduction. (A, D, and F) Results are mean ± SD. *P < 0.01 versus AxGFP-infected control. Scale bars: 500 μm.