Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 7-Day Trial for You or Your Team.

Learn More →

MACROPHAGE COLONY STIMULATING FACTOR RESTORES IN VIVO BONE RESORPTION IN THE OP/OP OSTEOPETROTIC MOUSE

MACROPHAGE COLONY STIMULATING FACTOR RESTORES IN VIVO BONE RESORPTION IN THE OP/OP OSTEOPETROTIC... The op/op variant of murine osteopetrosis is a recessive mutation characterized by impaired bone resorption due to lack of osteoclasts. Cultured osteoblasts and fibroblasts from this mutant do not secrete MCSF activity and resident macrophages are absent in bone marrow. This failure has been related to a mutation within the M-CSF coding region. We report now that the administration of recombinant human M-CSF (rhM-CSF) corrects in vivo the impaired bone resorption in this animal. The treatment restores the bone marrow cavity virtually absent in the op/op animal and induces the appearance of resorbing osteoclasts and of resident bone marrow macrophages. This proves that the deficiency of M-CSF is the cause of the op/op bone disorder and that this cytokine is directly or indirectly necessary for physiological osteoclastogenesis, the resulting bone resorption and for the establishment of bone marrow hemopoiesis. This content is only available as a PDF. Copyright © 1990 by The Endocrine Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Endocrinology Oxford University Press

MACROPHAGE COLONY STIMULATING FACTOR RESTORES IN VIVO BONE RESORPTION IN THE OP/OP OSTEOPETROTIC MOUSE

Endocrinology , Volume 127 (5) – Nov 1, 1990

Loading next page...
 
/lp/oxford-university-press/macrophage-colony-stimulating-factor-restores-in-vivo-bone-resorption-Kn3hfUzSqc

References (0)

References for this paper are not available at this time. We will be adding them shortly, thank you for your patience.

Publisher
Oxford University Press
Copyright
Copyright © 1990 by The Endocrine Society
ISSN
0013-7227
eISSN
1945-7170
DOI
10.1210/endo-127-5-2592
Publisher site
See Article on Publisher Site

Abstract

The op/op variant of murine osteopetrosis is a recessive mutation characterized by impaired bone resorption due to lack of osteoclasts. Cultured osteoblasts and fibroblasts from this mutant do not secrete MCSF activity and resident macrophages are absent in bone marrow. This failure has been related to a mutation within the M-CSF coding region. We report now that the administration of recombinant human M-CSF (rhM-CSF) corrects in vivo the impaired bone resorption in this animal. The treatment restores the bone marrow cavity virtually absent in the op/op animal and induces the appearance of resorbing osteoclasts and of resident bone marrow macrophages. This proves that the deficiency of M-CSF is the cause of the op/op bone disorder and that this cytokine is directly or indirectly necessary for physiological osteoclastogenesis, the resulting bone resorption and for the establishment of bone marrow hemopoiesis. This content is only available as a PDF. Copyright © 1990 by The Endocrine Society

Journal

EndocrinologyOxford University Press

Published: Nov 1, 1990

There are no references for this article.