Retinal dysfunction can be caused by aberrant neural cell migration during development. The understanding of collective migration and the role of signaling molecules critical to the developing retina remains incompletely understood. In this project, we examine the migration of neural cells of the third instar larvae of Drosophila Melanogaster through genetic manipulation of the GAL4-UAS expression system. Our experiments design microfluidic systems to model the chemotactic responses of glial and neuronal progenitors to extrinisic chemical factors and population density.
Müller Glia cells
Müller glia of the mammalian retina respond to injury via reactive gliosis, which can be either neuro-protective or neuro--disruptive. Retinal self-repair is limited in mammals, leading to cell death and visual disorders. Müller glia can attain progenitor-like characteristics in response to acute retinal injury or to exogenous growth factors, or beocme hypertrophic, migrate, and proliferate to form a glial scar. This project develops biomimmetic microfluidics to analyze the stimuli and behaviors of Müller glia in response to extrinsic chemical fields of exogenous ligands significant to the inner blood retinal barrier (iBRB).
retinal progenitor cells
Vision loss in adults with Age Related Macular Degeneration (AMD) is attributed to damage of photoreceptor cells that absorb and transduce light. Mouse models have suggested that transplantation of precursors may be a novel approach to restore vision. However, transplantation efficiency is exceedingly low due in large part to challenges with cell viability, infiltration into host retina, and synaptogenesis. This project uses a combination of electrotactic and chemotactic stimuli to guide the migration of photoreceptor replacemenets within microfluidic retinal models and explant systems.