MicroRNA-129-5p affects immune privilege and apoptosis of nucleus pulposus cells via regulating FADD in

Nan Li1, Qi Gao2,3, Wenli Zhou1

  • 1Department of Neonatology, The First Hospital of Jilin University, Changchun, Jilin, China.

Insights

MicroRNA-129-5p (miR-129-5p) protects against intervertebral disc degeneration (IDD) by reducing Fas-associated death domain (FADD) and inhibiting nucleus pulposus cell apoptosis.

Area of Science:

  • Biomedical Science
  • Molecular Biology
  • Regenerative Medicine

Background:

  • Intervertebral disc degeneration (IDD) is a significant cause of low back pain.
  • The roles of microRNA-129-5p (miR-129-5p) and Fas-associated death domain (FADD) in IDD are not fully understood.
  • Investigating the miR-129-5p/FADD axis is crucial for understanding IDD pathogenesis.

Purpose of the Study:

  • To investigate the effect of miR-129-5p on immune privilege and nucleus pulposus (NP) cell apoptosis in a rat model of IDD.
  • To determine if miR-129-5p regulates FADD expression in IDD.
  • To explore the therapeutic potential of miR-129-5p in IDD.

Main Methods:

  • Established a rat model of caudal IDD.
  • Administered miR-129-5p agomir or antagomir to IDD rats.
  • Assessed NP cell proliferation, apoptosis, and senescence.
  • Quantified apoptosis in macrophages and CD8+ cells.
  • Measured expression levels of miR-129-5p, FADD, collagen I, collagen II, aggrecan, and Sox-9.

Main Results:

  • Up-regulated miR-129-5p decreased FADD and collagen I, while increasing collagen II, aggrecan, and Sox-9 in NP tissues and cells.
  • miR-129-5p repressed inflammation in serum and NP tissues of IDD rats.
  • Elevated miR-129-5p promoted NP cell proliferation and apoptosis of macrophages and CD8+ cells, while inhibiting NP cell senescence and apoptosis.

Conclusions:

  • Up-regulated miR-129-5p exerts a protective effect on IDD by inhibiting NP cell apoptosis and promoting proliferation.
  • The mechanism involves the downregulation of FADD.
  • miR-129-5p also modulates immune responses by promoting macrophage and CD8+ cell apoptosis, suggesting its potential as a therapeutic target for IDD.

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