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

73 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

Access to Document

10.1016/S0898-6568(01)00221-2

Cite this

@article{81ff91828d194f038ef246e7abd3e56a,

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",

note = "Funding Information: We thank Dr. Y. Eto for recombinant human activin A, Dr. Tsurukai for recombinant human RANKL and Dr. G. Nunez for the reporter plasmids, Yamanouchi Pharmaceutical Co. Ltd. for recombinant human BMP-2. This work was supported in part by a Research on Health Science Focusing on Drug Innovation grant from The Japan Health Science Foundation (T.K., Y.G., N.O., T.N.) and by grants-in-aid from the Ministry of Education, Science and Culture of Japan (T.K., T.N.).",

year = "2002",

doi = "10.1016/S0898-6568(01)00221-2",

language = "English",

volume = "14",

pages = "31--36",

journal = "Cellular Signalling",

issn = "0898-6568",

publisher = "Elsevier Inc.",

number = "1",

}

TY - JOUR

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

N1 - Funding Information: We thank Dr. Y. Eto for recombinant human activin A, Dr. Tsurukai for recombinant human RANKL and Dr. G. Nunez for the reporter plasmids, Yamanouchi Pharmaceutical Co. Ltd. for recombinant human BMP-2. This work was supported in part by a Research on Health Science Focusing on Drug Innovation grant from The Japan Health Science Foundation (T.K., Y.G., N.O., T.N.) and by grants-in-aid from the Ministry of Education, Science and Culture of Japan (T.K., T.N.).

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.

KW - Activin A

KW - JunB

KW - Osteoclast

KW - RANKL

KW - TGF-β

KW - TRAP

KW - c-Src

UR - http://www.scopus.com/inward/record.url?scp=0036135923&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036135923&partnerID=8YFLogxK

U2 - 10.1016/S0898-6568(01)00221-2

DO - 10.1016/S0898-6568(01)00221-2

M3 - Article

C2 - 11747986

AN - SCOPUS:0036135923

VL - 14

SP - 31

EP - 36

JO - Cellular Signalling

JF - Cellular Signalling

SN - 0898-6568

IS - 1

ER -

Role of TGF-β family in osteoclastogenesis induced by RANKL

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this