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inner Blood Retinal Barrier (iBRB)

Breakdown of the retinal vascular network is the primary cause of progressive vision loss in diabetic retinopathy (DR). The selective physiological barrier, known as the inner blood retinal barrier (iBRB), consists of endothelial cells (ECs), the foot processes of Müller glia (MG), and a basal lamina that regulates the bilateral transport of nutrients, oxygen, and small molecules from the bloodstream into the retinal parenchyma. In diabetes, blood glucose leads to glycation of the iBRB basal lamina, which results in impaired protein function and damage to the iBRB integrity. This project investigates the synergistic relationship between MG and ECs to form an impermeable and integral physiological barrier, along with the effects of anti-VEGF drugs in MG behavior. 


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.

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).

Drosophila Melanogaster

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.

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