Ching Yuan, Ph.D.

Ching Yuan, Ph.D.
Assistant Professor
Director, Corneal Dystrophies Laboratory
Department of Ophthalmology
yuanx019@umn.edu

The main focus of our ongoing research is to investigate the pathogenesis mechanism and to develop potential therapeutic strategies for keratoepithelin (KE)-related corneal dystrophies. KE, an extracellular matrix protein, was first identified as a TGFb1-induced gene product (thereafter named as TGFbI or bigh-3) in a lung adenocarcinoma cell line. A recent study has linked the mutations of the KE gene (located in human chromosome 5q3l) to at least four types of cornea dystrophies (Avellino, granular, lattice type I and Reis-Bucklers).

Each year 50,000 people in the United States are newly diagnosed with stromal corneal dystrophies, inherited conditions with over 10 different phenotypes which potentially lead to vision impairment. These corneal dystrophies, such as lattice and granular dystrophies, are characterized by the presence of corneal opacities composed of amyloid or non-amyloid deposits and recurrent epithelial erosion. The severity of corneal dystrophies varies from asymptomatic to profound loss of vision. Corneal transplantations are often necessary to restore visual acuity. However, recurrence of corneal dystrophy on the grafts is often encountered. For example, it has been estimated that 15% of transplant recipients with lattice dystrophy, which is one of the more common stromal dystrophies, require a second corneal transplantation.  Currently, we are using state-of-the-art technologies such as RNA interference and DNA micro-array to delineate the roles of KE in maintaining the integrity of ocular surface. A pilot study, which includes gene therapy techniques on cultured corneal cells to correct the mutations of the KE gene, is currently underway. The information generated from our study will significantly facilitate future development of animal models and treatments for corneal dystrophies.