Osteoclast function is activated by osteoblastic cells through a mechanism involving cell-to-cell contact.

Osteoclast function is activated by osteoblastic cells through a mechanism involving cell-to-cell contact.
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破骨细胞功能由成骨细胞通过涉及细胞间接触的机制激活。

DOI:
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发表时间:
1996
期刊:
影响因子:
4.8
通讯作者:
T. Suda
T. Suda
中科院分区:
医学2区
文献类型:
--
作者:
E. Jimi;I. Nakamura;H. Amano;Y. Taguchi;T. Tsurukai;Tamura Makoto;N. Takahashi;T. Suda

文献摘要

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我们建立了一种从小鼠原代成骨细胞和骨髓细胞共培养中获得具有功能活性的破骨细胞样多核细胞(浓缩OCL)的浓缩制剂的方法。利用这些浓缩的OCL,通过两种方法检测成骨细胞对破骨细胞功能的影响:凹坑形成实验和肌动蛋白环形成实验。富集型OCL在牙本质片上培养24 h,仅形成少量吸收坑。当不同数量的原代成骨细胞被加入到浓缩的OCL中时,吸收坑的面积随着成骨细胞数量的增加而成比例地增加。与原代成骨细胞一样,已建立的成骨细胞系(MC3T3-E1和KS-4)和骨髓基质细胞系(MC3T3-G2/PA6和ST2)增强了富含OCLs引起的凹陷形成。成纤维细胞系NIH3T3和C3H10T1/2)和成肌细胞系C2C12未能激活OCL功能。当阻止MC3T3-E1细胞与富集型OCL细胞间的接触时,仅形成少量的吸收坑。在牙本质切片上加入MC3T3-E1细胞也能刺激富含破骨细胞的凹坑形成。无论是培养丰富的小鼠OCL细胞,还是在牙本质切片上培养真正的大鼠破骨细胞,肌动蛋白环的形成和凹坑形成活性都有很好的相关性。这些结果表明,破骨细胞的功能是由成骨细胞通过细胞与细胞和/或细胞与基质接触的机制激活的。
We have established a method for obtaining an enriched preparation of functionally active osteoclast-like multinucleated cells (enriched OCLs) from co-cultures of mouse primary osteoblasts and bone marrow cells. Using these enriched OCLs, the effect of osteoblastic cells on osteoclast function was examined in two assays: a pit formation assay and an assay for actin ring formation. The enriched OCLs cultured for 24 h on dentine slices formed only a few resorption pits. When various numbers of primary osteoblasts were added to the enriched OCLs, the areas of the resorption pits increased proportionally to the number of osteoblasts added. Like primary osteoblasts, the established cell lines of osteoblastic cells (MC3T3-E1 and KS-4) and bone marrow-derived stromal cells (MC3T3-G2/PA6 and ST2) potentiated the pit formation caused by enriched OCLs. In contrast, the fibroblastic cell lines NIH3T3 and C3H10T1/2) and the myoblastic cell line (C2C12) failed to activate OCL function. When cell-to-cell contact between MC3T3-E1 cells and enriched OCLs was prevented, only a few resorption pits were formed. Pit formation by enriched rat osteoclasts placed on dentine slices was also stimulated by adding MC3T3-E1 cells. Actin ring formation and pit forming activity were well correlated in either culture of enriched mouse OCLs or authentic rat osteoclasts on dentine slices. These results indicate that osteoclast function is activated by osteoblastic cells through a mechanism involving cell-to-cell and/or cell-to matrix contact.