Retinal dysfunction is caused by aberrant neural cell migration during development. The understanding of collective migration and the role of signaling molecules critical to the developing retina is misunderstood. In this study, we observe the migration of neural cells of the Drosophila Melanogaster aftermarking cells of the third instar larvae through genetic manipulation of the GAL4-UAS expression system. The primary objective is to mimic the neural chemotactic relationship of glial and neuronal progenitor cells to evaluate external chemotactic movement and population density.
Müller Glia cells
Müller glia cells are the most abundant cell type in the retina. In mammals Müller glia respond to injury in various ways that can be either protective or detrimental to retinal function. Regeneration and scar formation are the two main mechanisms how the retina repairs itself. However, in mammals retinal self-repair is limited leading to cell death and visual disorders. Müller glia can proliferate and attain progenitor-like characteristics in response to acute retinal injury or to exogenous growth factors. This project aims to analyze the stimuli and migration behavior of Müller glia in response to different concentrations of growth factors using a microfluidic device mimicking the in-vivo retinal environment.
retinal progenitor cells
Vision loss in adults with Age Related Macular Degeneration (AMD) is attributed to damage of retinal photoreceptor cells that initiate vision by absorbing light. Mouse models have suggested that transplantation of precursor cells may be a novel approach to restore vision. Outcomes project that the amount of restored visual response depends upon the migration of transplanted cells. However, transplantation efficiency is exceedingly low. This project uses a combination of electrotactic and chemotactic stimuli to promote and guide CNS cell migration within a microdevice model.