Increased Osteoclast Development After Estrogen Loss: Mediation by Interleukin-6

Osteoclasts, the cells that resorb bone, develop from hematopoietic precursors of the bone marrow under the control of factors produced in their microenvironment. The cytokine interleukin-6 can promote hematopoiesis and osteoclastogenesis. Interleukin-6 production by bone and marrow stromal cells is...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1992-07, Vol.257 (5066), p.88-91
Main Authors: Jilka, Robert L., Hangoc, Giao, Girasole, Giuseppe, Passeri, Giovanni, Williams, Daniel C., Abrams, John S., Boyce, Brendan, Broxmeyer, Hal, Manolagas, Stavros C.
Format: Article
Language:English
Subjects:
Analysis of the immune response. Humoral and cellular immunity
Analysis of Variance
Animals
Antibodies
Antibodies, Monoclonal
Biological and medical sciences
Bone marrow
Bone Marrow Cells
Bone resorption
Bones
Cells, Cultured
Cultured cells
Estradiol - pharmacology
Estrogens
Female
Fundamental and applied biological sciences. Psychology
Fundamental immunology
Granulocyte macrophage progenitor cells
Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology
Immunobiology
Immunoglobulin G
Interleukin-6
Interleukin-6 - immunology
Interleukin-6 - physiology
Lymphokines, interleukins ( function, expression)
Mice
Osteoclasts
Osteoclasts - cytology
Osteoclasts - drug effects
Ovariectomy
Physiological aspects
Recombinant Proteins - pharmacology
Regulatory factors and their cellular receptors
Spleen - cytology
Spleen cells
Stem Cells - cytology
Stem Cells - drug effects
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Summary:Osteoclasts, the cells that resorb bone, develop from hematopoietic precursors of the bone marrow under the control of factors produced in their microenvironment. The cytokine interleukin-6 can promote hematopoiesis and osteoclastogenesis. Interleukin-6 production by bone and marrow stromal cells is suppressed by 17β-estradiol in vitro. In mice, estrogen loss (ovariectomy) increased the number of colony-forming units for granulocytes and macrophages, enhanced osteoclast development in ex vivo cultures of marrow, and increased the number of osteoclasts in trabecular bone. These changes were prevented by 17β-estradiol or an antibody to interleukin-6. Thus, estrogen loss results in an interleukin-6-mediated stimulation of osteoclastogenesis, which suggests a mechanism for the increased bone resorption in postmenopausal osteoporosis.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.1621100