Link protein N-terminal peptide and fullerol promote matrix production and decrease degradation enzymes in rabbit annulus cells

Connect Tissue Res. 2018 Mar;59(2):191-200. doi: 10.1080/03008207.2017.1330333. Epub 2017 Jun 8.

Abstract

Purpose: Intervertebral disc degeneration is a major cause of back pain. Novel therapies for prevention or reversal of disc degeneration are needed. It is desirable for potential therapies to target both inflammation and matrix degeneration.

Materials and methods: The combined regenerative potential of link protein N-terminal peptide (LN) and fullerol on annulus fibrosus (AF) cells was evaluated in a 3D culture model.

Results: Interleukin-1α (IL-1α)-induced AF cell degeneration was counteracted by fullerol, LN, and fullerol + LN, with the latter having the greatest effect on matrix production as evaluated by real-time polymerase chain reaction and glycosaminoglycan assay. IL-1α-induced increases in pro-inflammatory mediators (interleukin-6 and cyclooxygenase-2) and matrix metalloproteinases (MMP-1, -2, -9, and -13) were also counteracted by fullerol and LN.

Conclusion: Our data demonstrate that LN and fullerol individually, and in combination, promote matrix production and have anti-inflammatory and anti-catabolic effects on AF cells.

Keywords: Back pain; fullerol; inflammation; intervertebral disc degeneration; link N peptide.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Annulus Fibrosus / metabolism*
  • Annulus Fibrosus / pathology
  • Collagenases / biosynthesis
  • Cyclooxygenase 2 / biosynthesis
  • Extracellular Matrix / metabolism*
  • Extracellular Matrix / pathology
  • Extracellular Matrix Proteins / pharmacology*
  • Fullerenes / pharmacology*
  • Interleukin-1alpha / biosynthesis
  • Interleukin-6 / biosynthesis
  • Intervertebral Disc Degeneration / drug therapy
  • Intervertebral Disc Degeneration / metabolism
  • Intervertebral Disc Degeneration / pathology
  • Male
  • Peptides / pharmacology*
  • Proteoglycans / pharmacology*
  • Rabbits

Substances

  • Extracellular Matrix Proteins
  • Fullerenes
  • Interleukin-1alpha
  • Interleukin-6
  • Peptides
  • Proteoglycans
  • link protein
  • Cyclooxygenase 2
  • Collagenases