# Induction and characterization of RGC axon regeneration in models of glaucoma

> **NIH NIH R21** · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · 2022 · $77,645

## Abstract

Induction and characterization of RGC axon regeneration in a mouse model of glaucoma
 Glaucoma is a large and heterogeneous group of optic neuropathies characterized by
optic nerve degeneration that results in irreversible vision loss. Primary open-angle glaucoma
(POAG) is the most common form of glaucoma, accounting for the majority of all cases.
Elevated intraocular pressure (IOP) is the most important and only known modifiable risk factor
associated with POAG. Despite therapeutic reduction of IOP, vision loss still continues to
progress in most glaucoma patients.
 Retinal ganglion cells (RGCs) are the only neurons that relay visual information from the
retina to the brain. Like other neurons in the central nervous system, RGCs do not
spontaneously regenerate their axons after damage. These neurons, which collectively form the
optic nerve, are also highly vulnerable when their axons are damaged. While the molecular
pathways that damage RGCs in glaucoma are not fully understood, several studies using the
animal models of glaucoma have described the presence of local insult in the optic nerve at the
level of lamina, where the RGC axons exit the eye. Furthermore, in a mouse model of glaucoma
(i.e. dexamethasone-induced ocular hypertension (OHT)), it was demonstrated that optic nerve
degeneration precedes structural and functional loss of RGCs, and that the axonal damage and
transport deficits initiate at the optic nerve head. Importantly, insults to the RGC axons under
these circumstances result in Wallerian degeneration distal to the site of damage, ultimately
causing disconnection between the retina and the brain.
 Using optic nerve crush in mice, we and others have demonstrated that genetic
manipulation of different genes in the RGCs promotes long distance axon regeneration.
However, while traumatic optic nerve crush is a useful technique for investigating the
mechanisms of RGC axon regeneration, it does not faithfully reproduce glaucomatous optic
nerve damage which axonal injury is partial and progresses gradually over time. In this
proposal, we will use a combination of axon tracing techniques, mouse genetics and 3D imaging
to examine the extent to which RGC axon regeneration and axon remodeling takes place after
OHT. The results obtained from this study will create a paradigm shift in how we investigate
optic nerve regeneration, and provide foundation for future investigations into developing
reparative therapy for treating advanced glaucoma patients.

## Key facts

- **NIH application ID:** 10468991
- **Project number:** 5R21EY033060-02
- **Recipient organization:** UNIVERSITY OF MIAMI SCHOOL OF MEDICINE
- **Principal Investigator:** KEVIN Kyung PARK
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $77,645
- **Award type:** 5
- **Project period:** 2021-09-01 → 2023-09-07

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10468991

## Citation

> US National Institutes of Health, RePORTER application 10468991, Induction and characterization of RGC axon regeneration in models of glaucoma (5R21EY033060-02). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10468991. Licensed CC0.

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