INCREASED OSTEOCLAST DEVELOPMENT AFTER ESTROGEN LOSS - MEDIATION BY INTERLEUKIN-6
INCREASED OSTEOCLAST DEVELOPMENT AFTER ESTROGEN LOSS - MEDIATION BY INTERLEUKIN-6
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DOI：
10.1126/science.1621100
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发表时间：
1992-07-03
期刊：
影响因子：
56.9
通讯作者：
MANOLAGAS, SC
中科院分区：
文献类型：
--
作者：
JILKA, RL;HANGOC, G;MANOLAGAS, SC
破骨细胞是吸收骨的细胞，在其微环境中产生的因子的控制下从骨髓的造血前体发育而来。细胞因子白细胞介素-6可以促进造血和破骨细胞生成。体外17-β-雌二醇抑制骨髓基质细胞产生白细胞介素-6在小鼠中，雌激素损失（卵巢切除术）增加了粒细胞和巨噬细胞的集落形成单位的数量，增强了骨髓体外培养中破骨细胞的发育，并增加了骨小梁中破骨细胞的数量。这些变化被17-β-雌二醇或白细胞介素-6抗体所阻止。因此，雌激素损失导致白细胞介素-6介导的破骨细胞生成刺激，这表明绝经后骨质疏松症中骨吸收增加的机制。
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 17-beta-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 17-beta-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.