Activation of focal adhesion kinase induces extracellular signal-regulated kinase-mediated osteogenesis in tensile force-subjected periodontal ligament fibroblasts but not in osteoblasts
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- 作者：Yi-Jyun Chen (1) (2) (4)
Ming-You Shie (3)
Chi-Jr Hung (1) (2)
Buor-Chang Wu (1) (2)
Shiau-Lee Liu (1) (2)
Tsui-Hsien Huang (1) (2)
Chia-Tze Kao (1) (2) - 关键词：Focal adhesion kinase (FAK) ; Tensile force ; Periodontal ligament (PDL) ; Osteoblast ; Osteogenic
- 刊名：Journal of Bone and Mineral Metabolism
- 出版年：2014
- 出版时间：November 2014
- 年：2014
- 卷：32
- 期：6
- 页码：671-682
- 全文大小：5,852 KB
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Chia-Tze Kao (1) (2)
1. School of Dentistry, Chung Shan Medical University, Taichung, 402, Taiwan
2. Department of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan
4. Dental Department, Taichung Hospital, Ministry of Health and Welfare, Taichung, Taiwan
3. Institute of Oral Science, Chung Shan Medical University, Taichung, Taiwan - ISSN：1435-5604
文摘
The exact mechanism by which focal adhesion kinase (FAK) translates mechanical signals into osteogenesis differentiation in force-subjected cells has not been elucidated. The responses to different forces differ according to the origin of cells and the type of stress applied. Therefore, the recruitment of osteoclast and osteoblast progenitor cells, and the balanced activation of these cells around and within the periodontal ligament (PDL) are essential for alveolar bone remodeling. Cells within the PDL and MG63 cells were subjected to tensile forces of ?00?kPa for different periods of time. At various times during the tensile force application, they were processed for the purpose of analyzing cell viability, cell cycle, and osteogenic protein. The effect of small interfering RNA transfection targeting FAK was also evaluated. Tensile force enhanced a rapid increase in the phosphorylation of FAK and up-regulated osteogenic protein expression in PDL cells, but not in MG63 cells. Transfecting PDL cells with FAK antisense oligonucleotide diminished alkaline phosphatase and osteocalcin secretion. These findings suggest that tensile force activates FAK pathways in PDL cells, which down-regulate immune cytokine and up-regulate osteogenic protein.