Open Access

Alterations in β‑catenin/E‑cadherin complex formation during the mechanotransduction of Saos‑2 osteoblastic cells

  • Authors:
    • Fei‑Fei Li
    • Bo Zhang
    • Ji‑Hong Cui
    • Fu‑Lin Chen
    • Yin Ding
    • Xue Feng
  • View Affiliations

  • Published online on: June 7, 2018     https://doi.org/10.3892/mmr.2018.9146
  • Pages: 1495-1503
  • Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Mechanical load application promotes bone formation, while reduced load leads to bone loss. However, the underlying mechanisms that regulate new bone formation are not fully understood. Wnt/β‑catenin signaling has an important role in bone formation, bone growth and remodeling. The aim of the present study was to investigate whether mechanical stimuli regulated bone formation through the Wnt/β‑catenin signaling pathway. Saos‑2 osteoblastic cells were subjected to mechanical strain using a Flexcell strain loading system. The results demonstrated that 12% cyclical tensile stress significantly stimulated Saos‑2 cell proliferation, increased the activity of alkaline phosphatase and promoted the formation of mineralized nodules, as determined by MTT and p‑nitrophenyl phosphate assays and Alizarin Red S staining, respectively. Furthermore, western blot analysis demonstrated that, following mechanical strain, increased phosphorylation of glycogen synthase kinase‑3β and nuclear β‑catenin expression was observed in cells, compared with static control culture cells. Results of reporter gene and reverse transcription‑polymerase chain reaction assays also demonstrated that mechanical strain significantly increased T‑cell factor reporter gene activity and the mRNA expression of cyclooxygenase (COX)‑2, cyclin D1, c‑fos and c‑Jun in Saos‑2 cells. Co‑immunoprecipitation analysis revealed that elongation mechanical strain activated Wnt/β‑catenin signaling and reduced β‑catenin and E‑cadherin interaction in Saos‑2 cells. In conclusion, the results of the current study indicate that mechanical strain may have an important role in the proliferation and differentiation of osteoblasts. The disassociation of the β‑catenin/E‑cadherin complex in the osteoblast membrane under stretch loading and the subsequent translocation of β‑catenin into the nucleus may be an intrinsic mechanical signal transduction mechanism.
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August-2018
Volume 18 Issue 2

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Li FF, Zhang B, Cui JH, Chen FL, Ding Y and Feng X: Alterations in β‑catenin/E‑cadherin complex formation during the mechanotransduction of Saos‑2 osteoblastic cells. Mol Med Rep 18: 1495-1503, 2018
APA
Li, F., Zhang, B., Cui, J., Chen, F., Ding, Y., & Feng, X. (2018). Alterations in β‑catenin/E‑cadherin complex formation during the mechanotransduction of Saos‑2 osteoblastic cells. Molecular Medicine Reports, 18, 1495-1503. https://doi.org/10.3892/mmr.2018.9146
MLA
Li, F., Zhang, B., Cui, J., Chen, F., Ding, Y., Feng, X."Alterations in β‑catenin/E‑cadherin complex formation during the mechanotransduction of Saos‑2 osteoblastic cells". Molecular Medicine Reports 18.2 (2018): 1495-1503.
Chicago
Li, F., Zhang, B., Cui, J., Chen, F., Ding, Y., Feng, X."Alterations in β‑catenin/E‑cadherin complex formation during the mechanotransduction of Saos‑2 osteoblastic cells". Molecular Medicine Reports 18, no. 2 (2018): 1495-1503. https://doi.org/10.3892/mmr.2018.9146