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

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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