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

American Association for the Advancement of Science (AAAS) - Tập 257 Số 5066 - Trang 88-91 - 1992
Robert L. Jilka1, Giao Hangoc2, G. Girasole3, Giovanni Passeri3, Daniel C. Williams4, J S Abrams5, Brendan F. Boyce6, Hal E. Broxmeyer7, Michaël R. Laurent3
1Department of Veterans Affairs Medical Center, Indiana University School of Medicine, Indianapolis 46202.
2Indiana Univ.-Purdue Univ. Indianapolis
3Indiana University, Bloomington
4Eli-Lilly.
5Merck
6University of Texas Health Science Center at San Antonio
7MICROBIOLOGY & IMMUNOLOGY

Tóm tắt

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.

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