Correlation between Adrenoceptor Expression and Clinical Parameters in Degenerated Lumbar Intervertebral Discs

Int J Mol Sci. 2022 Dec 5;23(23):15358. doi: 10.3390/ijms232315358.

Abstract

Despite advanced knowledge of the cellular and biomechanical processes of intervertebral disc degeneration (IVDD), the trigger and underlying mechanisms remain unclear. Since the sympathetic nervous system (SNS) has been shown to exhibit catabolic effects in osteoarthritis pathogenesis, it is attractive to speculate that it also influences IVDD. Therefore, we explored the adrenoceptor (AR) expression profile in human IVDs and correlated it with clinical parameters of patients. IVD samples were collected from n = 43 patients undergoing lumbar spinal fusion surgery. AR gene expression was analyzed by semi-quantitative polymerase chain reaction. Clinical parameters as well as radiological Pfirrmann and Modic classification were collected and correlated with AR expression levels. In total human IVD homogenates α1A-, α1B-, α2A-, α2B-, α2C-, β1- and β2-AR genes were expressed. Expression of α1A- (r = 0.439), α2A- (r = 0.346) and β2-AR (r = 0.409) showed a positive and significant correlation with Pfirrmann grade. α1A-AR expression was significantly decreased in IVD tissue of patients with adjacent segment disease (p = 0.041). The results of this study indicate that a relationship between IVDD and AR expression exists. Thus, the SNS and its neurotransmitters might play a role in IVDD pathogenesis. The knowledge of differential AR expression in different etiologies could contribute to the development of new therapeutic approaches for IVDD.

Keywords: Modic classification; Pfirrmann classification; adrenoceptor expression; intervertebral disc degeneration; spine; sympathetic nervous system.

MeSH terms

  • Humans
  • Intervertebral Disc Degeneration* / metabolism
  • Intervertebral Disc* / metabolism
  • Lumbar Vertebrae / metabolism
  • Lumbosacral Region
  • Magnetic Resonance Imaging
  • Receptors, Adrenergic / metabolism
  • Spinal Fusion*

Substances

  • Receptors, Adrenergic