Mechanical forces alter extracellular matrix synthesis by human periodontal ligament fibroblasts.

Mechanical forces alter extracellular matrix synthesis by human periodontal ligament fibroblasts.
复制标题

DOI:
10.1111/j.1600-0765.1998.tb02350.x
复制
发表时间:
2010-06
影响因子:
3.5
通讯作者:
Pamela S. Howard;Umberto Kucich;Rita Taliwal;Jonathan Korostoff
Pamela S. Howard;Umberto Kucich;Rita Taliwal;Jonathan Korostoff
中科院分区:
医学3区
文献类型:
--
作者:
Pamela S. Howard;Umberto Kucich;Rita Taliwal;Jonathan Korostoff

文献摘要

被引文献

相似文献

牙周膜成纤维细胞(PDLF)是一种异质细胞群,参与韧带和邻近硬组织的正常维护、修复和再生。此外,这些细胞对机械刺激作出反应的能力表明它们在介导生理和正畸牙齿移动基础的骨重塑方面发挥着核心作用。为了进一步表征它们在此过程中的作用,当前的研究评估了张力应力对人类 PDLF 细胞外基质 (ECM) 蛋白生物合成的影响。从提取的人前磨牙和第三磨牙中建立细胞株。与未拉伸对照相比,以 30 次/分钟的频率暴露于 5% 双轴变形(应变)24 小时的细胞表现出 I 型胶原和纤连蛋白合成的统计显着增加,以及原弹性蛋白产生的统计显着减少。暴露于 10% 应变的细胞对纤连蛋白和原弹性蛋白表现出相似的反应,而拉伸细胞合成的 I 型胶原蛋白的量与对照水平没有差异。这些结果表明,PDLF 的机械刺激改变了 I 型胶原、原弹性蛋白和纤连蛋白的产生,并且这些细胞对不同水平的机械应力有不同的反应。这些细胞响应特定强度的张力而改变 ECM 蛋白质合成的能力可能部分解释了 PDLF 如何调节韧带和硬组织重塑。
Periodontal ligament fibroblasts (PDLFs) are a heterogeneous population of cells that are involved in the normal maintenance, repair and regeneration of both the ligament and adjacent hard tissues. Additionally, the ability of these cells to respond to mechanical stimulation suggests that they have a central role in mediating the osseous remodeling that underlies physiological and orthodontic tooth movement. To characterize their role further in this process, the current study evaluated the effect of tensional stress on the biosynthesis of extracellular matrix (ECM) proteins by human PDLFs. Cell strains were established from extracted human premolars and third molars. Cells exposed to 5% biaxial deformation (strain) at a frequency of 30 times/min for 24 hr exhibited statistically significant increases in type I collagen and fibronectin synthesis, and a statistically significant decrease in tropoelastin production relative to unstretched controls. Cells exposed to 10% strain exhibited similar responses for fibronectin and tropoelastin while the amount of type I collagen synthesized by stretched cells did not differ from control levels. These results indicate that mechanical stimulation of PDLFs alters type I collagen, tropoelastin and fibronectin production and that these cells are differentially responsive to varying levels of mechanical stress. The ability of these cells to alter ECM protein synthesis in response to specific magnitudes of tensional stress may in part explain how PDLFs regulate ligament and hard tissue remodeling.