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

doi:10.1016/S0898-6568(01)00221-2

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 journal › Article › peer-review

68 Citations (Scopus)

Abstract

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 language	English
Pages (from-to)	31-36
Number of pages	6
Journal	Cellular Signalling
Volume	14
Issue number	1
DOIs	https://doi.org/10.1016/S0898-6568(01)00221-2
Publication status	Published - 2002
Externally published	Yes

Keywords

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

ASJC Scopus subject areas

Cell Biology

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title = "Role of TGF-β family in osteoclastogenesis induced by RANKL",

abstract = "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.",

keywords = "Activin A, JunB, Osteoclast, RANKL, TGF-β, TRAP, c-Src",

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

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T1 - Role of TGF-β family in osteoclastogenesis induced by RANKL

AU - Koseki, Takeyoshi

AU - Gao, Ying

AU - Okahashi, Nobuo

AU - Murase, Yoshiyuki

AU - Tsujisawa, Toshiyuki

AU - Sato, Tsuyoshi

AU - Yamato, Kenji

AU - Nishihara, Tatsuji

PY - 2002

Y1 - 2002

N2 - 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.

AB - 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.

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KW - TGF-β

KW - TRAP

KW - c-Src

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