Role of TGF-β family in osteoclastogenesis induced by RANKL

Takeyoshi Koseki, Ying Gao, Nobuo Okahashi, Yoshiyuki Murase, Toshiyuki Tsujisawa, Tsuyoshi Sato, Kenji Yamato, Tatsuji Nishihara

Research output: Contribution to journalArticlepeer-review

73 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)31-36
Number of pages6
JournalCellular Signalling
Issue number1
Publication statusPublished - 2002


  • Activin A
  • JunB
  • Osteoclast
  • TGF-β
  • TRAP
  • c-Src


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