Department of Ophthalmology

University of Michigan

Ann Arbor, MI

BASIC RESEARCH PROJECT

Control of neurogenesis during retinal development

Research Interests

The irreversible loss of retinal neurons underlies the pathology of many blinding diseases, such as macular degeneration, retinitis pigmentosa and glaucoma. Therefore, effective cell-based therapies that can replenish the se cells via cell transplantation or endogenous reprogramming are urgently needed. To achieve this goal, it is crucial to gain a deep understanding of the gene regulatory networks and mechanisms that control the generation of different retinal cell types. Over the course of retinal development, retinal progenitors progressively generate diverse types of retinal neurons and Müller glia. However, the molecular mechanisms that control this process remain largely unclear.

Plans for 2025

This study aims to identify the role of transcription factor Insm1 during mouse retinal development and regeneration. Our study will enhance our current understanding of how different retinal cell types are produced, as well as help guide cell based therapies aimed at replacing retinal neurons.

In 2025, Dr. Hoang’s laboratory will aim to characterize the molecular and electrophysiological properties of regenerated neurons from Insm1-overexpressing Muller glia.

Specific Aims:
Aim1. Molecular characterization of neurons derived from Insm1-overexpressing Muller glia
Aim2. Electrophysiological characterization of neurons derived from Insm1 overexpressing Muller glia

Progress in 2024

During 2024, Dr. Hoang performed retinal-specific deletion of Insm1 during mouse development, and found that loss of Insm1 did not result in an obvious defect in retinal cell type formation. However, Insm1 deletion resulted in progressive retinal degeneration and gliosis. Furthermore, Dr. Hoang also found that Insm1 overexpression substantially enhances the regeneration of neurons from Notch signaling-deficient Muller glia cells in adult mice.