HEAT-TREATED OSTEOBLASTIC CELL (ROS17/2.8)-CONDITIONED MEDIUM INDUCES THE FORMATION OF OSTEOCLAST-LIKE CELLS

HEAT-TREATED OSTEOBLASTIC CELL (ROS17/2.8)-CONDITIONED MEDIUM INDUCES THE FORMATION OF OSTEOCLAST-LIKE CELLS
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DOI:
10.1016/s0169-6009(08)80048-7
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发表时间:
1993-11-01
期刊:
BONE AND MINERAL
影响因子:
--
通讯作者:
KOHASHI, O
KOHASHI, O
中科院分区:
其他
文献类型:
--
作者:
KUKITA, A;KUKITA, T;KOHASHI, O

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目的:研究成骨细胞产品对骨损伤的影响。我们将大鼠成骨细胞系ROS17/2.8的条件培养基(CM)添加到大鼠骨髓培养中,在10(-8)M 1,25-二羟基维生素D-3 (1,25(OH)(2)D-3)存在下形成抗酒石酸酸性磷酸酶(TRAP)阳性的破骨细胞样多核细胞(MNCs)。培养第7天,1,25(OH)(2) d -3依赖性trap阳性MNC的形成被ROS1712.8细胞cm (ROSCM)的bbb10 kDa组分强烈抑制,但热处理的ROSCM (htROSCM)对MNC的形成表现出明显的刺激。与单用1,25(OH)(2)D-3诱导的MNCs相比,htROSCM和1,25(OH)(2)D-3诱导的MNCs中几种破骨细胞表型的表达增强。htROSCM和1,25(OH)(2)D-3诱导的MNCs具有高运动性,对降钙素(CT)敏感,骨吸收活性高。这些数据表明,在大鼠骨髓培养系统中,在1,25(OH)(2)D-3存在的情况下,htROSCM促进破骨细胞分化。htROSCM中trap阳性MNC形成的刺激活性来源于热稳定蛋白,该蛋白被认为不同于集落刺激因子(csf),如巨噬细胞- csf (M-CSF)或粒细胞-巨噬细胞- csf (GM-CSF)。
To study the effects of osteoblast products on. osteoclast formation, we added the conditioned medium (CM) of rat osteoblastic cell line ROS17/2.8 to rat bone marrow cultures, in which tartrate-resistant acid phosphatase (TRAP)-positive osteoclast-like multinucleate cells (MNCs) formed in the presence of 10(-8) M 1,25-dihydroxyvitamin D-3 (1,25(OH)(2)D-3). The formation of 1,25(OH)(2)D-3-dependent TRAP-positive MNC at day 7 of culture was strongly inhibited by the >10 kDa fraction of ROS1712.8 cell-CM (ROSCM), but heat treated ROSCM (htROSCM) expressed marked stimulation in the formation of the MNCs. The expression of several osteoclastic phenotypes of the MNCs induced by htROSCM and 1,25(OH)(2)D-3 was more enhanced compared with that of the MNCs induced by 1,25(OH)(2)D-3 alone. The MNCs induced by htROSCM and 1,25(OH)(2)D-3 were highly motile, were sensitive to calcitonin (CT), and had high bone resorbing activity. These data suggest that htROSCM promotes the osteoclast differentiation in the presence of 1,25(OH)(2)D-3 in a rat bone marrow culture system. The stimulatory activity of TRAP-positive MNC formation in htROSCM is derived from heat-stable protein(s) that is (are) thought to be different from colony-stimulating factors (CSFs) such as macrophage-CSF (M-CSF) or granulocyte-macrophage-CSF (GM-CSF).