The role of cell signaling defects on the proliferation of osteoblasts on the calcium phosphate apatite thin film

The role of cell signaling defects on the proliferation of osteoblasts on the calcium phosphate apatite thin film
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DOI:
10.1016/j.biomaterials.2006.02.032
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发表时间:
2006-07-01
期刊:
影响因子:
14
通讯作者:
Kim, HM
Kim, HM
中科院分区:
工程技术1区
文献类型:
--
作者:
Lee, YJ;Ko, JS;Kim, HM

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在体外研究了结晶不良的磷酸钙磷灰石晶体(PCA)薄膜上控制成骨细胞增殖的细胞内信号转导。使用磷酸盐缓冲钙离子溶液在聚苯乙烯培养皿或盖玻片上制备PCA薄膜,通过加热低温制备的不饱和溶液使其过饱和。 PCA薄膜无需额外的表面处理即可用于细胞培养。在细胞培养皿上铺板的细胞与在 PCA 表面上培养的细胞之间发现了一些差异。进入细胞周期S期明显延迟,成骨细胞增殖率低。在PCA薄膜上,细胞以更细长的形状铺展。此外,使用免疫细胞化学染色检查发现,PCA 上的细胞中粘着斑和应力纤维的形成明显较弱。粘着斑激酶(FA K)的激活也较低。细胞周期蛋白 D1 和 E 的表达也较低。 Ras-细胞外信号调节激酶 (ERK)-MAP 激酶信号通路在血清刺激下被微弱激活。这些结果表明,PCA 表面上的低细胞增殖似乎是由于迫使细胞周期进行的信号传导不足所致,这可能是由于该表面上的细胞粘附信号传导较弱所致。 (c) 2006 Elsevier Ltd. 保留所有权利。
The intracellular signal transduction controlling the proliferation of osteoblastic cells on a thin film of poorly crystalline calcium phosphate apatite crystals (PCA) was studied in vitro. The PCA thin film was prepared on polystyrene culture dishes or cover glasses using phosphate-buffered calcium ion solution, which was made oversaturated by heating an undersaturated solution prepared at low temperature. The PCA thin film was used for cell culture without additional surface treatment. Several differences were found between the cells plated on a cell culture dish and the cells cultured on the PCA Surface. Entry into S-phase of the cell cycle was markedly delayed and there was a low proliferation rate of osteblast. On the PCA thin film, the cells spread in a more slender shape. Also, the formation of focal adhesions and stress fibers, examined using immunocytochemical staining, was strikingly weaker in the cells on PCA. The activation of focal adhesion kinase (FA K) was low as well. Expression of cyclins D1 and E was also lower. The Ras-Extracellular signal-regulated kinase (ERK)-MAP kinase signaling pathway was weakly activated by stimulation with serum. These results demonstrate that the low cell proliferation on the PCA surface appears to be due to insufficient activation of signaling that forces the cell cycle to progress and this may be due to weak adhesion signaling in cells on that surface. (c) 2006 Elsevier Ltd. All rights reserved.