On Tuesday, January 31, the Department of Biology sponsored a lecture titled “Visualizing Retinal Regeneration – When Development isn’t Good Enough.” Featured lecturer Dr. Travis Bailey, an assistant professor at State University of New York (SUNY) at Geneseo and close friend of Colgate’s Associate Professor of Biology and Neuroscience and University Studies Jason Meyers, spoke of his entry into the field of regenerative biology and his ongoing research at SUNY Geneseo. His research explores the stimulation of stem cells in the retina as a novel therapeutic avenue for vision loss.
“When I was your age, I was thinking about how I could get into regenerative biology. [But] there was nothing out there. No one was doing it. No research. No research programs,” Bailey said, regarding the state of the field only a few decades prior.
Although the field of retinal regeneration was largely nonexistent at the start of Bailey’s career, he explained the ease with which government support quickly brought retinal regeneration to the forefront of the research community. As Bailey explained, since most politicians are over the age of sixty and experiencing a variable degree of vision loss, the field hits closer to home. As a result, research surrounding Age-Related Macular Degeneration, glaucoma, diabetic retinopathy and other diseases associated with vision loss have been well supported.
Currently, therapies addressing vision loss are focused on reducing or halting the progression of retinal degeneration. Dr. Bailey and his colleagues are determined to pave a new therapeutic avenue: stimulating an endogenous response in the retina to trigger the proliferation of new photoreceptor cells and effectively reverse vision loss.
Using zebrafish as a developmental model system, Bailey and his team are investigating the ability of Müller glia cells to act as stem cells. Although primarily known for protecting neurons, glial cells can also regenerate photoreceptor loss. As Bailey described, these glial cells are able to gauge retinal damage and respond by dividing to produce progenitors that proliferate, migrate and differentiate into new photoreceptor cells. Bailey explained how his team was working with this process and the results they were looking to produce.
“How is regeneration need communicated? We were hoping to discover the presence of a positive signal generated by the damaged retina that could be manipulated to trigger regeneration,” Bailey explained.
That was exactly what they found. Through gene expression profiles, 2D protein gel and microarray, Bailey identified TNF as a gene upregulated to respond to retinal damage. In order to examine the therapeutic value of this revelation, Bailey attempted to stimulate a regenerative response in Müller glial cells by giving undamaged retina TNF(alpha) in the form of morpholinos. Unfortunately, TNF(alpha) was not sufficient to produce an endogenous response. While Bailey and his team did prove that TNF(alpha) is required for retinal regeneration in zebrafish, other factors are also needed to stimulate a long-lasting regenerative response.
Bailey and his team are currently looking to identify these additional required factors. If Bailey and his research team are successful in manipulating the regenerative response of Müller glial cells, aging individuals will not only be able to halt vision loss but rather regain the vision of their youth. As vision deterioration is a ubiquitous component of aging, the lives of most individuals would be transformed.
Additionally, the benefits of this new therapeutic avenue would extend to include other fields of pathogenesis. Senior neuroscience student Meghan McHale is currently conducting her thesis on Multiple Sclerosis (MS). McHale attended the lecture and was very enthusiastic about the potential of Dr. Bailey’s work.
“This research has huge implications for MS and other neurodegenerative diseases. Since optic neuritis is one of the early indicators of MS onset, this research may provide insight in understanding the fundamental etiology of MS pathogenesis,” McHale said.