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Article Open Access

N‑cadherin attenuates nucleus pulposus cell senescence under high‑magnitude compression

  • Authors:
    • Ming Niu
    • Fei Ma
    • Jun Qian
    • Junwei Li
    • Tong Wang
    • Yuzhen Gao
    • Jian Jin
  • View Affiliations / Copyright

    Affiliations: The Second Department of Surgery, Ganzhou People's Hospital, Zhangye, Gansu 734000, P.R. China, The First Department of Orthopaedic Surgery, Zhangye People's Hospital Affiliated to Hexi University, Zhangye, Gansu 734000, P.R. China, Department of Spine Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China
    Copyright: © Niu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2879-2884
    |
    Published online on: December 11, 2017
       https://doi.org/10.3892/mmr.2017.8239
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Abstract

Mechanical compression is important in disc degeneration. N-cadherin (N-CDH)-mediated signaling contributes to the maintenance of the normal nucleus pulposus (NP) cell phenotype and NP matrix biosynthesis. Our preliminary study demonstrated that a high‑magnitude compression (20% deformation) promotes NP cell senescence in a three‑dimensional scaffold culture system. The aim of the present study was to investigate whether N‑CDH‑mediated signaling alleviates NP cell senescence under the above‑mentioned high‑magnitude compression. NP cells were transfected with recombinant lentiviral vectors to enhance N‑CDH expression. All the transfected or un‑transfected NP cells were seeded into the scaffolds and subjected to 20% deformation at a frequency of 1.0 Hz for 4 h once per day for 5 days. Results indicated that N‑CDH overexpressed NP cells exhibited decreased senescence‑associated β‑galactosidase activity and downregulated expression levels of senescence‑associated markers (p16 and p53). Furthermore, the N‑CDH overexpressed NP cells exhibited increased cell proliferation potency, telomerase activity and matrix biosynthesis compared with NP cells without N‑CDH overexpression under high‑magnitude compression. Thus, N‑CDH‑mediated signaling contributes to the attenuation of NP cell senescence under high‑magnitude compression.
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Copy and paste a formatted citation
Spandidos Publications style
Niu M, Ma F, Qian J, Li J, Wang T, Gao Y and Jin J: N‑cadherin attenuates nucleus pulposus cell senescence under high‑magnitude compression. Mol Med Rep 17: 2879-2884, 2018.
APA
Niu, M., Ma, F., Qian, J., Li, J., Wang, T., Gao, Y., & Jin, J. (2018). N‑cadherin attenuates nucleus pulposus cell senescence under high‑magnitude compression. Molecular Medicine Reports, 17, 2879-2884. https://doi.org/10.3892/mmr.2017.8239
MLA
Niu, M., Ma, F., Qian, J., Li, J., Wang, T., Gao, Y., Jin, J."N‑cadherin attenuates nucleus pulposus cell senescence under high‑magnitude compression". Molecular Medicine Reports 17.2 (2018): 2879-2884.
Chicago
Niu, M., Ma, F., Qian, J., Li, J., Wang, T., Gao, Y., Jin, J."N‑cadherin attenuates nucleus pulposus cell senescence under high‑magnitude compression". Molecular Medicine Reports 17, no. 2 (2018): 2879-2884. https://doi.org/10.3892/mmr.2017.8239
Copy and paste a formatted citation
x
Spandidos Publications style
Niu M, Ma F, Qian J, Li J, Wang T, Gao Y and Jin J: N‑cadherin attenuates nucleus pulposus cell senescence under high‑magnitude compression. Mol Med Rep 17: 2879-2884, 2018.
APA
Niu, M., Ma, F., Qian, J., Li, J., Wang, T., Gao, Y., & Jin, J. (2018). N‑cadherin attenuates nucleus pulposus cell senescence under high‑magnitude compression. Molecular Medicine Reports, 17, 2879-2884. https://doi.org/10.3892/mmr.2017.8239
MLA
Niu, M., Ma, F., Qian, J., Li, J., Wang, T., Gao, Y., Jin, J."N‑cadherin attenuates nucleus pulposus cell senescence under high‑magnitude compression". Molecular Medicine Reports 17.2 (2018): 2879-2884.
Chicago
Niu, M., Ma, F., Qian, J., Li, J., Wang, T., Gao, Y., Jin, J."N‑cadherin attenuates nucleus pulposus cell senescence under high‑magnitude compression". Molecular Medicine Reports 17, no. 2 (2018): 2879-2884. https://doi.org/10.3892/mmr.2017.8239
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