# Muller glia: roles in retinal homeostasis and neuronal regeneration

> **NIH NIH R01** · OHIO STATE UNIVERSITY · 2020 · $390,000

## Abstract

Project Summary: There is a rapidly growing body of evidence that Müller glia can are a source of retinal
progenitors to promote neural regeneration. Many studies have demonstrated that Müller glia can become
proliferating progenitor cells in the retinas of different vertebrate species. Most reports have studied Müller
glia-derived progenitors in acutely damaged retinas. However, little is known about the mechanisms that
stimulate neurogenesis from Müller glia-derived progenitors in undamaged retinas or retinas undergoing slow,
progressive degeneration. Furthermore, the regeneration of retinal neurons in warm-blooded vertebrates is
limited compared to that seen in cold-blooded vertebrates. Therefore, the identification of the secreted factors
and signaling pathways that permit and/or stimulate neural regeneration from Müller glia-derived progenitors is
crucially important to developing new therapies to treat degenerative diseases of the human retina. We have
obtained compelling novel preliminary data indicating that cell-signaling through the nuclear factor kappa-light-
chain-enhancer of activated B cells (NFκB) and the activity of Enhancer of Zeste Homolog 2 (EZH2) impacts
the de-differentation and reprogramming of Müller glia into proliferating, neurogenic retinal progenitors. We will
investigate how the phenotype and plasticity of the Müller glia are regulated by NFκB and EZH2 in normal,
damaged and growth factor-treated retinas. We will use a combination of pharmacological and genetic
approaches to selectively activate or inhibit NFκB and EZH2 in Müller glia. We will compare and contrast how
NFκB-signaling and EZH2-acitvity impact the formation of Müller glia-derived progenitors in chick and rodent
model systems with different inherent capacities for retinal regeneration. We expect that the completion of the
experiments described in this proposal will provide significant new information regarding how NFκB and EZH2
influence mature Müller glia, the formation of Müller glia-derived progenitors and regeneration of retinal
neurons. Identification and understanding of the mechanisms that enhance the neurogenic potential of Müller
glia is required to develop new therapies for sight-threatening diseases, such as glaucoma and macular
degeneration that involve the loss of retinal neurons.

## Key facts

- **NIH application ID:** 10019557
- **Project number:** 5R01EY022030-08
- **Recipient organization:** OHIO STATE UNIVERSITY
- **Principal Investigator:** ANDY J FISCHER
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $390,000
- **Award type:** 5
- **Project period:** 2012-08-01 → 2022-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10019557

## Citation

> US National Institutes of Health, RePORTER application 10019557, Muller glia: roles in retinal homeostasis and neuronal regeneration (5R01EY022030-08). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10019557. Licensed CC0.

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