Expression of neural and neurotrophic markers in nucleus pulposus cells isolated from degenerated intervertebral disc

J Orthop Res. 2012 Sep;30(9):1470-7. doi: 10.1002/jor.22098. Epub 2012 Feb 28.

Abstract

Intervertebral disc (IVD) degeneration is a common disorder of the lower spine. Since it is caused by loss of cellularity, there is interest in the comprehension of the cellular phenotypes. This study aimed to verify if stem cells isolated from nucleus pulposus of intervertebral discs (NPs-IVD), which may express neurogenic properties, may be implicated in IVD disease. NPs-IVD isolated from 14 human pathological discs were cultured under mesenchymal and neural differentiation. An induction of the neural markers GFAP, NF, MAP2, O4, and a decrement of the expression of the immature neural markers β-tubulin III, Nestin, NG2, occurred within the neural differentiation. The expression of TrkA and p75NGFR, the receptors of NGF, was not correlated with neural induction; in contrast, TrkB, the BDNF receptor, increased and was co-expressed with acid sensing ion channel 3 (ASIC3). In the same condition, neuroinflammatory markers were over-expressed. We confirm our hypothesis that stem cells within IVD degeneration acquire neurogenic phenotype, causing the induction of markers related to inflammatory condition. These cells could promote the enrolment of neurotrophines in adaptation to the acidic microenvironment in degenerative conditions. These data could improve our knowledge about IVD cellularity and eventually lead to the development of pharmacological therapies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acid Sensing Ion Channels
  • Biomarkers / metabolism*
  • Female
  • Humans
  • Intervertebral Disc / cytology
  • Intervertebral Disc / metabolism*
  • Intervertebral Disc Degeneration / metabolism*
  • Male
  • Mesenchymal Stem Cells / metabolism*
  • Microtubule-Associated Proteins / metabolism
  • Nerve Tissue Proteins / metabolism*
  • Neurogenesis
  • Phenotype
  • Receptor, trkA / metabolism
  • Receptor, trkB / metabolism
  • Sodium Channels / metabolism

Substances

  • ASIC3 protein, human
  • Acid Sensing Ion Channels
  • Biomarkers
  • MAP2 protein, human
  • Microtubule-Associated Proteins
  • Nerve Tissue Proteins
  • Sodium Channels
  • Receptor, trkA
  • Receptor, trkB