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Updated: May 1, 2026

Microfluidic Chip for Axonal Injury Models Construction and Enabling Multi-Omics Analysis
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RNA sequence reveals mouse retinal transcriptome changes early after axonal injury.

Masayuki Yasuda1, Yuji Tanaka1, Morin Ryu1

  • 1Department of Ophthalmology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Plos One
|March 29, 2014
PubMed
Summary

Glaucoma involves retinal ganglion cell (RGC) death from axonal injury. This study reveals endoplasmic reticulum stress, antioxidant, and immune responses are key early molecular mechanisms in RGC injury.

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Area of Science:

  • Ophthalmology
  • Neuroscience
  • Molecular Biology

Background:

  • Glaucoma is characterized by progressive retinal ganglion cell (RGC) death due to axonal injury.
  • The precise molecular mechanisms driving RGC death after axonal injury are not fully understood.

Purpose of the Study:

  • To investigate the early-stage transcriptome profile and molecular pathways following axonal injury in a mouse model.
  • To identify key biological processes involved in RGC death after optic nerve crush.

Main Methods:

  • Utilized RNA sequencing (RNA-seq) technology to analyze retinal gene expression in mice after optic nerve crush (ONC) or sham procedures.
  • Performed pathway analysis to identify significant upstream regulators and biological pathways.

Main Results:

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  • Identified 177 differentially expressed genes, including significantly upregulated endoplasmic reticulum (ER) stress genes (e.g., Atf3, Chop, Egr1).
  • ATF4 was identified as a significant upstream regulator.
  • Upregulation of antioxidative response genes (Hmox1, Srxn1) and immune response genes (C1qa, C1qb, C1qc) was observed.

Conclusions:

  • Endoplasmic reticulum stress plays a critical role in the early stages of RGC injury following axonal damage.
  • Concurrent activation of antioxidative and immune responses occurs early after axonal injury.
  • This study provides novel insights into the molecular mechanisms underlying RGC death in glaucoma.