Omentin-1 promoted proliferation and ameliorated inflammation, apoptosis, and degeneration in human nucleus pulposus cells

Arch Gerontol Geriatr. 2022 Sep-Oct:102:104748. doi: 10.1016/j.archger.2022.104748. Epub 2022 Jun 9.

Abstract

Purpose: Intervertebral disc degeneration is an abnormal, cell-mediated process of tissue remodeling, recognized as the principal cause of low back pain affecting 80% of the population worldwide. Inflammatory cytokine, Interleukin-1beta (IL-1β) is involved in the intervertebral disc degeneration (IDD) process, and it is upregulated in degenerated discs. Omentin-1, also known as intelectin-1, is an adipokine with anti-inflammatory, anti-apoptosis, pro-proliferation, and proangiogenic properties in various types of cells. However, little is known about the effects of omentin-1 on human nucleus pulposus cells (HNPCs). This study aims to investigate the effects of omentin-1 on healthy HNPCs regarding proliferation and further investigate the effects of omentin-1 on IL-1β-induced inflammation, apoptosis, and degeneration in HNPCs.

Methods: Genes and proteins of interest were measured by qRT-PCR, immunoblotting, and immunofluorescence to conduct related experiments. Cell viability (CCK-8), EdU, and mitochondrial membrane potential (JC-1), flow cytometry assays were used to assess proliferation and apoptosis, respectively.

Results: Our study showed that omentin-1 promoted proliferation in normal HNPCs. Furthermore, omentin-1 expression was decreased in IL-1β-treated HNPCs. Omentin-1 protected against IL-1β-induced inflammation, apoptosis, and degeneration in HNPCs in vitro via the activation of the PI3K/Akt signaling pathway.

Conclusion: These findings may contribute to understanding the role of omentin-1 in HNPCs and may be a potential therapeutic candidate for intervertebral disc degeneration.

Keywords: Adipokines; Human nucleus pulposus cells; Intervertebral disc degeneration; Omentin-1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Proliferation
  • Cytokines* / genetics
  • Cytokines* / metabolism
  • GPI-Linked Proteins / genetics
  • GPI-Linked Proteins / metabolism
  • Humans
  • Inflammation / metabolism
  • Intervertebral Disc Degeneration* / genetics
  • Intervertebral Disc Degeneration* / metabolism
  • Lectins* / genetics
  • Lectins* / metabolism
  • Nucleus Pulposus* / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism

Substances

  • Cytokines
  • GPI-Linked Proteins
  • ITLN1 protein, human
  • Lectins