Activation of FAK promotes ERK-mediated osteogenesis for tensile force-subjected periodontal ligament cell

Ze-Jian Li, Chunting Lu, Shu Y. Ma, Ren-fa Lai, Jiong Li
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Abstract

The exact mechanism of translate mechanical signals of the focal adhesion kinase (FAK) into osteoblast differentiation power. PDL cells and MG63 cells were under-100 kPa for different periods. The tension force of focal adhesion kinase (FAK) phosphorylation increases rapidly and upregulation of osteogenic protein expression in periodontal ligament cells, but not in MG63 cells with FAK antisense oligonucleotides decreased ALP and Osteocalcin (OC) secretion in cells transfected with PDL. These findings suggest that the tension of the activation of the FAK pathway in periodontal ligament cells, and regulate immune cytokines and regulation of bone morphogenetic protein.
FAK的激活促进erk介导的牙周韧带细胞的成骨作用
聚焦黏附激酶(FAK)机械信号转化成骨细胞分化能力的确切机制。PDL细胞和MG63细胞在不同时期均处于100 kPa以下。局灶黏附激酶(FAK)磷酸化的张力在牙周韧带细胞中迅速增加,成骨蛋白表达上调,而FAK反义寡核苷酸转染后的MG63细胞中ALP和骨钙素(OC)分泌减少。这些发现提示,张力激活了牙周膜细胞中的FAK通路,并调节免疫细胞因子和骨形态发生蛋白的调节。
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