Macrophage-inflammatory protein-1alpha regulates preosteoclast differentiation in vitro

Research output: Contribution to journalArticlepeer-review

Standard

Macrophage-inflammatory protein-1alpha regulates preosteoclast differentiation in vitro. / Scheven, B A; Milne, J S; Hunter, I; Robins, S P.

In: Biochemical and Biophysical Research Communications, Vol. 254, No. 3, 1999, p. 773-8.

Research output: Contribution to journalArticlepeer-review

Harvard

APA

Vancouver

Author

Bibtex

@article{24f48558cba14d4e809716b1df7d9665,
title = "Macrophage-inflammatory protein-1alpha regulates preosteoclast differentiation in vitro",
abstract = "A validated in vitro system was used to investigate the nature of osteoclast-inducing growth factors (OGF) present in fetal rat calvarial conditioned medium (RCCM). Evidence is presented here that macrophage inflammatory protein-1alpha (MIP-1alpha), a member of the C-C chemokine family, is an essential factor for the induction of osteoclast differentiation in this system. Specific polyclonal antibodies against MIP-1alpha significantly inhibited development of TRAP-positive osteoclast precursors and multinucleated osteoclasts induced by RCCM. Anti-MIP-1alpha antibody treatment was accompanied by an increase in the number of macrophage-like cells, suggesting that bone-derived MIP-1alpha is involved in the direction of preosteoclast formation with an inhibitory action on progenitor cell proliferation. Reverse-phase HPLC of RCCM resolved multiple fractions with OGF activity. OGF fractions separated at low acetonitrile (AcN) concentrations (",
author = "Scheven, {B A} and Milne, {J S} and I Hunter and Robins, {S P}",
note = "Copyright 1999 Academic Press.",
year = "1999",
doi = "10.1006/bbrc.1998.9909",
language = "English",
volume = "254",
pages = "773--8",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Elsevier",
number = "3",

}

RIS

TY - JOUR

T1 - Macrophage-inflammatory protein-1alpha regulates preosteoclast differentiation in vitro

AU - Scheven, B A

AU - Milne, J S

AU - Hunter, I

AU - Robins, S P

N1 - Copyright 1999 Academic Press.

PY - 1999

Y1 - 1999

N2 - A validated in vitro system was used to investigate the nature of osteoclast-inducing growth factors (OGF) present in fetal rat calvarial conditioned medium (RCCM). Evidence is presented here that macrophage inflammatory protein-1alpha (MIP-1alpha), a member of the C-C chemokine family, is an essential factor for the induction of osteoclast differentiation in this system. Specific polyclonal antibodies against MIP-1alpha significantly inhibited development of TRAP-positive osteoclast precursors and multinucleated osteoclasts induced by RCCM. Anti-MIP-1alpha antibody treatment was accompanied by an increase in the number of macrophage-like cells, suggesting that bone-derived MIP-1alpha is involved in the direction of preosteoclast formation with an inhibitory action on progenitor cell proliferation. Reverse-phase HPLC of RCCM resolved multiple fractions with OGF activity. OGF fractions separated at low acetonitrile (AcN) concentrations (

AB - A validated in vitro system was used to investigate the nature of osteoclast-inducing growth factors (OGF) present in fetal rat calvarial conditioned medium (RCCM). Evidence is presented here that macrophage inflammatory protein-1alpha (MIP-1alpha), a member of the C-C chemokine family, is an essential factor for the induction of osteoclast differentiation in this system. Specific polyclonal antibodies against MIP-1alpha significantly inhibited development of TRAP-positive osteoclast precursors and multinucleated osteoclasts induced by RCCM. Anti-MIP-1alpha antibody treatment was accompanied by an increase in the number of macrophage-like cells, suggesting that bone-derived MIP-1alpha is involved in the direction of preosteoclast formation with an inhibitory action on progenitor cell proliferation. Reverse-phase HPLC of RCCM resolved multiple fractions with OGF activity. OGF fractions separated at low acetonitrile (AcN) concentrations (

U2 - 10.1006/bbrc.1998.9909

DO - 10.1006/bbrc.1998.9909

M3 - Article

C2 - 9920817

VL - 254

SP - 773

EP - 778

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 3

ER -