Recent studies have revealed that both transforming growth factor-β (TGF-β) and activin A play pivotal roles in osteoclastogenesis. In this report, we show that the effect of TGF-β family members, TGF-β1 and activin A, but not BMP-2, enhance multinucleated osteoclast-like cell (OCL) formation induced by receptor activator of NF-κB ligand (RANKL) in isolated bone marrow macrophages and monocytic cell line, RAW264.7. TGF-β1 and activin A caused the growth suppression and concomitant expression of tartrate-resistant acid phosphatase (TRAP) and c-Src, without inducing syncytium formation or increasing the survival rate in RAW264.7 cells. Although TGF-β1 and activin A had no effect on NF-κB and JNK activities, these factors enhanced the expression of JunB, a component of the AP-1 transcriptional complex. These results suggest that TGF-β1 and activin A may function as commitment factors in osteoclastic differentiation, not as a crucial component for terminal differentiation to form multinucleated OCLs nor in OCL survival.
ASJC Scopus subject areas