Ameilia Chung
Pronouns: she/her
Research Mentor(s): Thanh Hoang
Research Mentor School/College/Department: Ophthalmology and CDB / Medicine
Program:
Authors: Thanh Hoang, Zachary Flickinger, Nadia Kress, Ameilia Chung
Session: Session 6: 3:40 pm – 4:30 pm
Poster: 97
Abstract
Loss of retinal neurons underlies the pathology of many retinal degenerations, including retinitis pigmentosa, age-macular degeneration and glaucoma. Some non-mammalian vertebrates, such as zebrafish, Xenopus and chick, are able to regenerate a diverse set of retinal neurons via reprogramming of Müller glia (MG) cells. In contrast, in mammals such as mice and humans, MG do not spontaneously regenerate lost retinal neurons following injury. Therefore, the identification of the cellular and molecular mechanisms underlying MG-mediated regeneration will facilitate the development of cell-based therapies for human retinal degeneration. We previously reconstructed transcriptional regulatory networks that control MG injury response and reprogramming across multiple species. We showed that inhibition of the NFI family transcription factors Nfia/b/x and Notch signaling pathways resulted in MG proliferation and robust generation of retinal interneurons: bipolar and amacrine, and a limited number of rod photoreceptors in adult mouse retinas. The goal of this study is to determine whether different injury models could lead to the regeneration of different retinal neurons from MG cells. To test this, NFI/Rbpj-deficient mice will be subjected to two injury models: light damage and NMDA injection which ablate photoreceptors and retinal amacrine/ ganglion cells, respectively. The identity of regenerated neurons will be determined by immunohistochemistry. We expect that MG will show differential regenerative responses between the two injury models. Understanding the mechanism of how different cell types are regenerated will inform us the development of a novel cell-based therapy to restore vision in retinal degenerative diseases.
