Our Research 

Understanding molecular mechanisms of preventing RGC death, re-establishing neuronal wiring and recovering visual functions, leads to providing new targets for preventive and therapeutic interventions for traumatic optic neuropathy and glaucoma.

Clues?
Boosting axon regrowth 

From a high-throughput in vitro axonal regeneration assay, small molecules have been identified to overcome inhibitory cues for axonal outgrowth of several types of neurons (Li, Kuwajima et al.,2016). These molecular targets could be involved in axonal 

regrowth after nerve injury.

Extrinsic molecular signals 

After nerve injury and in neurodegenerative diseases, non-neuronal cells such as glial cells affect neuronal survival or death and axon regeneration. Among them, myelin debris-induced signals inhibit RGC axon regeneration (Li, Kuwajima et al.,2016). Other molecular signals from glial cells could affect each regenerative step.

Reprogramming RGCs 

During development, retinal axon growth and guidance are regulated by multiple guidance molecules and transcription factors (Mason et al., 2013, Book chapter). These molecules could be key mediators for axon regeneration and rewiring after injury.

Funding
Research to Prevent Blindness/Ernest & Elizabeth Althouse/Dolly Green Special Scholar Award
UPMC Competitive Medical Research Fund
Department of Ophthalmology, University of Pittsburgh