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Updated: Dec 29, 2025

Experimental Strategies to Bridge Large Tissue Gaps in the Injured Spinal Cord after Acute and Chronic Lesion
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Experimental Strategies to Bridge Large Tissue Gaps in the Injured Spinal Cord after Acute and Chronic Lesion

Published on: April 5, 2016

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A novel hydrogel-based treatment for complete transection spinal cord injury repair is driven by

Dezun Ma1, Yannan Zhao2, Lei Huang3

  • 1State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, 100101, PR China; University of Chinese Academy of Sciences, Beijing, 100101, PR China.

Biomaterials
|February 10, 2020
PubMed

Insights

Combined therapy targeting microglia/macrophage inflammation after spinal cord injury (SCI) promotes neural stem/progenitor cell (NSPC) neurogenesis and functional recovery. This approach reduces inflammation and enhances neuron generation in the injured spinal cord.

Area of Science:

  • Neuroscience
  • Regenerative Medicine
  • Immunology

Background:

  • Microglia/macrophage-mediated inflammation is a key factor hindering spinal cord injury (SCI) repair.
  • The impact of this inflammation on the neurogenic differentiation of endogenous neural stem/progenitor cells (NSPCs) remains unclear.

Purpose of the Study:

  • To investigate the effects of combined therapy on microglia/macrophage-mediated inflammation in SCI.
  • To assess the promotion of endogenous NSPC neurogenesis and functional recovery following this combined treatment.

Main Methods:

  • Utilized a combination of photo-crosslinked hydrogel transplantation and CSF1R inhibitor (PLX3397) to deplete and repopulate microglia/macrophages in complete transection SCI mice.
  • Quantified reactive microglia/macrophages (CD68-positive) and pro-inflammatory factor mRNA levels.
  • Employed genetic fate mapping (Nestin-CreERT2; LSL-tdTomato) to trace the origin of newly generated neurons (Tuj1-positive).

Main Results:

  • The combined treatment significantly reduced CD68-positive microglia/macrophages and pro-inflammatory markers compared to single treatments.
  • A substantial increase in Tuj1-positive neurons was observed in the lesion area post-treatment.
  • Genetic fate mapping confirmed that newly formed neurons originated from endogenous NSPCs.

Conclusions:

  • Combined inhibition of microglia/macrophage-mediated inflammation promotes endogenous NSPC neurogenesis in SCI.
  • This therapeutic strategy offers a promising approach for improving functional recovery after complete transection SCI.
Keywords:
Complete transection spinal cord injury (SCI)InflammationMicroglia/macrophagesNeurogenesisPhoto-crosslinked gelatin hydrogel

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