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Updated: Jun 3, 2026
Rat Model of Photochemically-Induced Posterior Ischemic Optic Neuropathy
Published on: November 29, 2015
Expression change of PirB in mice retina after optic nerve injury
1Department of Ophthalmology, First Clinical College of Harbin Medical University, Harbin 150001, P.R. China.
Abstract:
The aim of this study was to observe the location of paired immunoglobulin-like receptor B (PirB) in the retina and to evaluate the expressive varieties of PirB in the retina of mice after optic nerve injury. In situ hybridization was used to observe the location of PirB mRNA in the retina of mice. Western blotting was used to analyze the levels of PirB protein in retina 7 days after optic nerve crush. Expression of PirB was located in the retinal ganglion cells of mice. The level of PirB protein increased significantly in the retina after optic nerve crush compared to the control group. PirB plays an important role in the inhibition of axonal regeneration after optic nerve injury. We conclude that the inhibition of PirB expression may enhance axonal regeneration after optic nerve traumas.
Insights
Paired immunoglobulin-like receptor B (PirB) is found in mouse retinal ganglion cells. Optic nerve injury increases PirB protein levels, inhibiting axonal regeneration.
Area of Science:
- Neuroscience
- Ophthalmology
- Regenerative Medicine
Background:
- Paired immunoglobulin-like receptor B (PirB) is implicated in neuronal development and plasticity.
- Understanding PirB's role in the retina is crucial for developing strategies to promote vision recovery after injury.
Purpose of the Study:
- To determine the localization of PirB within the mouse retina.
- To investigate changes in PirB expression following optic nerve injury.
Main Methods:
- In situ hybridization to visualize PirB mRNA.
- Western blotting to quantify PirB protein levels post-optic nerve crush.
Main Results:
- PirB expression was confirmed in retinal ganglion cells.
- A significant increase in PirB protein levels was observed 7 days after optic nerve crush compared to controls.
- PirB was identified as an inhibitory factor for axonal regeneration.
Conclusions:
- PirB is present in retinal ganglion cells and its expression is upregulated after optic nerve injury.
- Inhibiting PirB may represent a promising therapeutic strategy to enhance axonal regeneration and restore vision after optic nerve trauma.
