FUSION DISABILITY OF EMBRYONIC OSTEOCLAST PRECURSOR CELLS AND MACROPHAGES IN THE MICROPHTHALMIC OSTEOPETROTIC MOUSE
FUSION DISABILITY OF EMBRYONIC OSTEOCLAST PRECURSOR CELLS AND MACROPHAGES IN THE MICROPHTHALMIC OSTEOPETROTIC MOUSE
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DOI：
10.1016/8756-3282(85)90406-5
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发表时间：
1985-01-01
期刊：
影响因子：
4.1
通讯作者：
SCHERFT, JP
中科院分区：
文献类型：
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作者：
THESINGH, CW;SCHERFT, JP
研究人员对小眼骨石化 (mi) 小鼠从胚胎早期到新生儿阶段的破骨细胞形成进行了研究。胚胎和胎儿mi/mi破骨细胞是在长骨中形成骨髓之前的时期产生的，主要是单核并且缺乏褶皱边界。然而，这些细胞确实显示出许多破骨细胞的形态和功能特性，例如丰富的线粒体、琥珀酸脱氢酶和酸性磷酸酶反应呈阳性，以及与钙化软骨基质的密切接触和吸收（尽管有所减少）。这些破骨细胞单核细胞出现在体内以及胎儿跖骨及其完整骨膜的器官培养物中。在无骨膜的胎儿跖骨与破骨细胞前体的几种外来来源的共培养中也观察到了它们：9天和11天胚胎的卵黄囊和腹部区域、胎儿肝脏以及从胎儿肝脏中分离的预培养的单核吞噬细胞。相反，+/+破骨细胞总是多核的，在吸收钙化软骨基质方面功能正常，并且在体内以及来自上述来源时具有褶皱边界。与植入的 Melinex 片上肉芽肿中的 +/+ 巨噬细胞相反，胎儿肝脏来源的 mi/mi 巨噬细胞也未能形成多核异物巨细胞。来自胚胎和胎儿髓外mi/mi单核细胞/巨噬细胞来源的细胞的融合失败与来自年轻mi/mi小鼠骨髓前体的多核破骨细胞和异物巨细胞的发生形成对比。我们得出的结论是，mi/mi 破骨细胞前体细胞的融合缺陷已经存在于非常年轻胚胎的血细胞形成器官的祖先中，并且这些细胞分化成单核破骨细胞，在产前骨骼中功能低下。我们推测，在发育完全的骨髓中，局部因素有利于消除融合缺陷。
Osteoclast formation in the microphthalmic osteopetrotic (mi) mouse was studied from very early embryonic to newborn stages. Embryonic and fetal mi/mi osteoclasts, generated during the period before bone marrow is formed in the long bones, were predominatly mononuclear and lacked ruffled borders. These cells, did, however, show many osteoclastic morphologic and functional properties, such as an abundance of mitochondia, positive succinic dehydrogenase and acid phosphatase reactions, and close contact with and resorption of the calcified cartilage matrix (though diminished). These osteoclastic mononuclear cells appeared in vivo as well as in organ cultures of fetal metatarsal bones with their intact periostea. They also were observed in co-cultures of periosteum-free fetal metatarsal bones, with several extraneous sources of osteoclast precursors: yolk sacs and abdominal regions of 9- and 11-day-old embryos, fetal livers, and precultured mononuclear phagocytes isolated from the fetal liver. In contrast, +/+ osteoclasts were always multinuclear, functioned normally in resorbing the calcified cartilage matrix, and had ruffled borders in vivo as well as when derived from the above-mentioned sources. Fetal liver-derived mi/mi macrophages also failed to form multinuclear foreign body giant cells as opposed to +/+ macrophages in granulomas on implanted pieces of Melinex. The fusion failure of cells derived from embryopnic and fetal extramedullary mi/mi monocyte/macrophage sources contrasted with the occurrence of multinuclear osteoclasts and foreign body giant cells derived from precursors from the bone marrow in young mi/mi mice. We conclude that the fusion defect of mi/mi osteoclast precursor cells is already present in their ancestry in blood cell-forming organs of very young embryos and that these cells differentiate into mononuclear osteoclasts that function inefficiently in prenatal bone. We presume that in fully developed bone marrow, local factors are favorable for abolishing the fusion defect.