Colony-stimulating factors regulate the development of multinucleated osteoclasts from recently replicated cells in vitro.
Colony-stimulating factors regulate the development of multinucleated osteoclasts from recently replicated cells in vitro.
复制标题
集落刺激因子调节来自体外最近复制的细胞的多核破骨细胞的发育。
DOI：
10.1172/jci113042
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Medlock,ES
中科院分区：
文献类型：
--
作者：
Lorenzo,JA;Sousa,SL;Fonseca,JM;Hock,JM;Medlock,ES
破骨细胞在骨吸收过程中起重要作用。然而，人们对破骨细胞或破骨细胞前体形成的调控机制知之甚少。相比之下，集落刺激因子(CSF)调节髓系细胞及其前体的形成是众所周知的。由于破骨细胞和髓样细胞可能起源于共同的干细胞，我们研究了两种CSF，粒细胞-巨噬细胞集落刺激因子(GM-CSF)和白介素3(IL-3)对骨吸收、破骨细胞形成以及最近复制的核进入小鼠骨培养的破骨细胞的影响。CSFS对破骨细胞形成率或其吸收活性影响不大，但显着降低甲状旁腺激素处理组破骨细胞中新近复制的破骨细胞前体细胞的百分比。GM-CSF还增加了培养的骨髓间隙中的髓样细胞的数量，以及这些细胞来自最近复制的祖细胞的比例。这些结果表明，GM-CSF和IL-3可以调节新近复制的胎鼠长骨前体细胞向破骨细胞的发育。然而，CSF影响破骨细胞形成的机制很难从这些研究中确定，因为破骨细胞前体和前体的标志物不存在。这些数据还提供了证据，表明破骨细胞前体细胞的分化在其个体发育的不同阶段受到不同因素的调节。
Osteoclasts mediate the process of bone resorption. However, little is known about the mechanisms that regulate the formation of either osteoclasts or osteoclast precursors. In contrast, colony-stimulating factors (CSFs) are well-known to regulate the formation of myeloid cells and their precursors. Because osteoclasts and myeloid cells may originate from a common stem cell, we examined the effects of two CSFs, granulocyte-macrophage CSF (GM-CSF) and interleukin 3 (IL-3), on bone resorption, osteoclast formation, and the incorporation of recently replicated nuclei into the osteoclasts of mouse bone cultures. CSFs had little effect on the formation rate of osteoclasts or their resorptive activity but significantly decreased the percentage of recently replicated osteoclast progenitor cell nuclei present in the osteoclasts of bones treated with parathyroid hormone. GM-CSF also increased the number of myeloid cells in the marrow space of the cultures and the percentage of these cells derived from recently replicated progenitors. These results demonstrate that GM-CSF and IL-3 can regulate the development of osteoclasts from recently replicated precursor cells in cultured fetal mouse long bones. However, the mechanisms by which CSFs influence osteoclast formation are difficult to determine from these studies because markers for the osteoclast progenitor and precursor do not exist. These data also provide evidence that the differentiation of osteoclast progenitors is regulated by different factors at different points in their ontogeny.