Wnt5a suppresses inflammation-driven intervertebral disc degeneration via a TNF-α/NF-κB-Wnt5a negative-feedback loop

Osteoarthritis Cartilage. 2018 Jul;26(7):966-977. doi: 10.1016/j.joca.2018.04.002. Epub 2018 Apr 12.

Abstract

Objective: This study was to investigate the molecular role of Wnt5a on inflammation-driven intervertebral disc degeneration (IVDD).

Methods: The expression of Wnt5a was analyzed in human nucleus pulposus (NP) tissues with immunohistochemical staining. The effects of Wnt5a on matrix production were assessed by RT-qPCR and western blotting. Small interfering RNAs (siRNAs), promoter deletion assay, and promoter binding site mutant were used to reveal the molecular role of Wnt5a in TNF-α-induced matrix metalloproteinase (MMP) expression. The regulatory effects of TNF-α on Wnt5a were investigated with pharmachemical inhibitors and siRNA experiment.

Results: The expression of Wnt5a was elevated in moderately degenerated human NP tissue with similar expression pattern of TNF-α. In NP cells, Wnt5a significantly increased aggrecan and collagen II expression. Inhibition of JNK or interfering Sox9 gene expression significantly suppressed Wnt5a-induced matrix production. AP-1(JunB) binding sites were located in Sox9 promoter and mutation of these sites sabotaged Wnt5a-induced Sox9 up-regulation and subsequent matrix genes expression. Notably, Wnt5a, which was induced by TNF-α, on the other way round suppressed TNF-α-NF-κB (p65) signaling and subsequent MMPs expression. In vivo studies with MR imaging confirmed the protective role of Wnt5a in IVDD.

Conclusions: Wnt5a, which can be induced by TNF-α, increased matrix production in a Sox9-dependent manner through the activation of JNK-AP1 (JunB) signaling, and antagonized TNF-α-induced up-regulation of MMPs through the inhibition of NF-κB signaling. It indicates that Wnt5a suppresses IVDD through a TNF-α/NF-κB-Wnt5a negative-feedback loop.

Keywords: Intervertebral disc degeneration; Negative feedback loop; Nucleus pulposus; TNF-α; Wnt5a.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Aggrecans / genetics
  • Binding Sites / genetics
  • Biopsy, Needle
  • Female
  • Gene Expression Regulation*
  • Humans
  • Immunohistochemistry
  • Inflammation / genetics
  • Intervertebral Disc Degeneration / genetics*
  • Intervertebral Disc Degeneration / pathology*
  • Magnetic Resonance Imaging / methods
  • Male
  • Matrix Metalloproteinases / metabolism
  • Middle Aged
  • Nucleus Pulposus / pathology
  • Real-Time Polymerase Chain Reaction / methods
  • Retrospective Studies
  • Signal Transduction / genetics
  • Tissue Embedding
  • Transcription Factor RelA / genetics
  • Transcriptional Activation / genetics
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Up-Regulation
  • Wnt-5a Protein / genetics*

Substances

  • Aggrecans
  • RELA protein, human
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • WNT5A protein, human
  • Wnt-5a Protein
  • Matrix Metalloproteinases