Tumor necrosis factor alpha promotes the proliferation of human nucleus pulposus cells via nuclear factor-κB, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinase

Exp Biol Med (Maywood). 2015 Apr;240(4):411-7. doi: 10.1177/1535370214554533. Epub 2014 Oct 10.

Abstract

Although tumor necrosis factor alpha (TNF-α) is known to play a critical role in intervertebral disc (IVD) degeneration, the effect of TNF-α on nucleus pulposus (NP) cells has not yet been elucidated. The aim of this study was to explore the effect of TNF-α on proliferation of human NP cells. NP cells were treated with different concentrations of TNF-α. Cell proliferation was determined by cell counting kit-8 (CCK-8) analysis and Ki67 immunofluorescence staining, and expression of cyclin B1 was studied by quantitative real-time RT-PCR. Cell cycle was measured by flow cytometry and cell apoptosis was analyzed using an Annexin V-fluorescein isothiocyanate (FITC) & propidium iodide (PI) apoptosis detection kit. To identify the mechanism by which TNF-α induced proliferation of NP cells, selective inhibitors of major signaling pathways were used and Western blotting was carried out. Treatment with TNF-α increased cell viability (as determined by CCK-8 analysis) and expression of cyclin B1 and the number of Ki67-positive and S-phase NP cells, indicating enhancement of proliferation. Consistent with this, NP cell apoptosis was suppressed by TNF-α treatment. Moreover, inhibition of NF-κB, c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) blocked TNF-α-stimulated proliferation of NP cells. In conclusion, the current findings suggest that the effect of TNF-α on IVD degeneration involves promotion of the proliferation of human NP cells via the NF-κB, JNK, and p38 MAPK pathways.

Keywords: Tumor necrosis factor alpha; intervertebral disc degeneration; mitogen-activated protein kinase; nuclear factor-κB; nucleus pulposus cell; proliferation.

MeSH terms

  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Cell Cycle / drug effects
  • Cell Cycle / physiology
  • Cell Proliferation / drug effects*
  • Cell Proliferation / physiology
  • Cells, Cultured
  • Cyclin B1 / metabolism
  • Dose-Response Relationship, Drug
  • Humans
  • Intervertebral Disc / cytology*
  • Intervertebral Disc / drug effects
  • Intervertebral Disc / physiology
  • JNK Mitogen-Activated Protein Kinases / physiology*
  • MAP Kinase Signaling System / drug effects
  • MAP Kinase Signaling System / physiology
  • NF-kappa B / physiology*
  • Signal Transduction / drug effects
  • Signal Transduction / physiology
  • Tumor Necrosis Factor-alpha / pharmacology*
  • p38 Mitogen-Activated Protein Kinases / physiology*

Substances

  • Cyclin B1
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • JNK Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases