The Fox Center for Vision Restoration organizes an exciting lecture series focusing on ocular regeneration and new therapies.
Distinguished national and international speakers present their innovative and multidisciplinary approaches to finding cures for vision impairment. The objective of this lecture series is to accelerate research through knowledge sharing, partnership building and out of the box thinking.
Awakening the dormant regenerative potential of the mammalian retina
Dong Feng Chen, PhD, MD
Associate Professor of Ophthalmology, The Schepens Eye Research Institute, Harvard Medical School
September 5, 11:45am – 1:00pm
Lunch will be served at 11:30am.
(Please RSVP to firstname.lastname@example.org)
Dr. Chen is a graduate of Beijing University School of Medicine and was trained in the laboratory of Nobel laurel Dr. Susumu Tonegawa at the Massachusetts Institute of Technology. She is an RPB Sybil B. Harrington Scholar and recipiant of Outstanding Scientific Achievement Award from RP International.
Dr. Chen's research focuses on mechanisms and application of neuroregenerative approach for retinal and central nervous system repair. Her lab is the first to demonstrate full-length optic nerve regeneration in mice and to discover the molecules that can awaken the sleeping progenitor cells to repair the retina.
Please check this link for more information.
In adult mammals, neurons in the central nervous system (CNS) exhibit limited ability for regeneration. Isolation of multipotent progenitor cells from the adult CNS suggests that their neurogenic potential is dictated by local environmental cues. We report that the retina and brain of adult mice express high levels of ephrin-A2 and -A3, which present an inhibitory niche, negatively regulating progenitor cell growth. While the ciliary epithelium (CE) of adult mammals has been reported to provide a source of retinal stem cells (RSCs) that can give rise to all retinal cell types in vitro, we show that the neurogenic potential of CE-derived cells is negatively regulated by ephrin-A3. Addition of ephrin-A3 inhibits proliferation of CE-derived RSCs and increases pigment epithelial cell fate. In contrast, absence of ephrin-A3 promotes proliferation and increases expression of neural progenitor cell markers and photoreceptor progeny. The negative effects of ephrin-A3 on CE-derived RSCs are mediated through activation of an EphA4 receptor and suppression of Wnt3a/ -catenin signaling. Together, our results suggest that manipulating ephrin and Wnt/ -catenin signaling may represents a viable approach to activating the endogenous neurogenic potential of RSCs for treating retinal degenerative disorders.
Location and Address
Eye and Ear Boardroom, 5th floor, Eye and Ear Institute
203 Lothrop Street, Pittsburgh PA 15213