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The Regulatory Effect of MicroRNA-101-3p on Disc Degeneration by the STC1/VEGF/MAPK Pathway

Juehan Wang1, Leizhen Huang1, Xi Yang1

  • 1Department of Orthopedic Surgery and Orthopedic Research Institute, West China Hospital, Sichuan University, No. 37 Guoxue Road, Chengdu, Sichuan, China.

Oxidative Medicine and Cellular Longevity
|October 15, 2021
PubMed

Insights

MicroRNA-101-3p, a key molecule, is downregulated in intervertebral disc degeneration (IDD). Restoring its levels inhibits apoptosis and alleviates IDD progression by targeting the STC1/VEGF/MAPK pathway.

Area of Science:

  • Biomedical Research
  • Molecular Biology
  • Regenerative Medicine

Background:

  • Intervertebral disc degeneration (IDD) is a significant cause of back pain, with microRNAs (miRNAs) implicated in its pathogenesis.
  • Understanding novel miRNA regulatory mechanisms is crucial for developing effective IDD therapies.

Purpose of the Study:

  • To identify and characterize the role of specific miRNAs in IDD.
  • To elucidate the molecular mechanisms underlying miRNA-mediated regulation in IDD.
  • To evaluate the therapeutic potential of targeting miRNAs for IDD treatment.

Main Methods:

  • MicroRNA microarray analysis of human degenerated and normal disc samples.
  • Quantitative real-time PCR (qRT-PCR) to validate miRNA expression.
  • In vitro cell culture and in vivo rat models for functional studies.
  • Bioinformatic analysis to predict and confirm miRNA-target interactions.

Main Results:

  • miR-101-3p expression was significantly decreased in degenerated discs and correlated with IDD severity.
  • Upregulation of miR-101-3p inhibited cell apoptosis and suppressed the expression of stanniocalcin-1 (STC1), vascular endothelial growth factor (VEGF), and the MAPK pathway.
  • Administration of agomir-101-3p in an IDD rat model demonstrated a therapeutic effect in suspending disc degeneration.

Conclusions:

  • miR-101-3p plays a protective role in intervertebral disc degeneration.
  • The therapeutic potential of miR-101-3p warrants further investigation for IDD treatment.
  • Targeting the STC1/VEGF/MAPK pathway via miR-101-3p offers a novel therapeutic strategy for IDD.

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