MicroRNA-21-5p promotes the inflammatory response after spinal cord injury by targeting PLAG1

K Han1, F-R Wang, M-Q Yu

  • 1Department of Traumatic Orthopaedics, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China. sdslyygkhk@126.com.

Abstract

Insights

MicroRNA-21-5p is upregulated in spinal cord injury (SCI) patients and promotes inflammation by targeting PLAG1. This study investigated its role in SCI-related microglial inflammation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • Spinal cord injury (SCI) triggers significant neuroinflammation.
  • MicroRNAs play crucial roles in regulating cellular processes, including inflammation.
  • Understanding the molecular mechanisms of SCI pathogenesis is vital for developing effective treatments.

Purpose of the Study:

  • To investigate the expression of microRNA-21-5p and its target gene PLAG1 in spinal cord injury (SCI) patients.
  • To elucidate the role and mechanism of microRNA-21-5p in lipopolysaccharide (LPS)-induced primary microglial inflammation.
  • To explore the potential therapeutic targets for SCI-related inflammation.

Main Methods:

  • Quantitative Polymerase Chain Reaction (qPCR) was used to measure microRNA-21-5p and PLAG1 levels in patient serum and cell models.
  • Enzyme-linked immunosorbent assay (ELISA) quantified inflammatory factors (IL-1, IL-6, TNF-α).
  • Luciferase reporter assay confirmed the binding relationship between microRNA-21-5p and PLAG1.

Main Results:

  • MicroRNA-21-5p was upregulated in SCI patients' serum and LPS-treated microglial cells.
  • PLAG1 expression was downregulated in SCI patients and negatively correlated with microRNA-21-5p.
  • Knockdown of microRNA-21-5p or overexpression of PLAG1 reduced inflammatory cytokine levels.

Conclusions:

  • MicroRNA-21-5p promotes microglial inflammation in the context of spinal cord injury.
  • The mechanism involves the targeting of PLAG1 by microRNA-21-5p.
  • MicroRNA-21-5p represents a potential therapeutic target for mitigating SCI-induced inflammation.

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