Douglas Rhee, M.D.

   


Douglas Rhee, M.D.
Department Chair
University Hospitals
Department of Ophthalmology and Visual Sciences
11100 Euclid Avenue, Lakeside 4126
Cleveland, Ohio 44106
Phone: (216) 844-8590 Fax: (216) 983-0524
Email: douglas.rhee@uhhospitals.org
Research Focus: Glaucoma

Research Summary

Dr. Douglas J. Rhee arrived at the University Hospitals Eye Institute in 2013 and serves as the Chair of the Department of Ophthalmology and Visual Sciences.  He is a glaucoma specialist, molecular biologist, and board-certified ophthalmologist.  Previously, he had served at the Massachusetts Eye & Ear Infirmary (MEEI) (ranked 4th by US News and World Report), Children’s Hospital Boston (CHB) and was an associate professor at Harvard Medical School.  Prior to MEEI and CHB, Dr. Rhee was an attending physician at Wills Eye Hospital (ranked 2nd by US News and World Report) and was an assistant professor at Jefferson Medical College in both the departments of Ophthalmology and Pathology, Anatomy, and Cell Biology.

His laboratory group simultaneously investigates the mechanisms of ECM synthesis and turnover in the trabecular meshwork (TM).  Modulation of extracellular matrix (ECM) in the trabecular meshwork (TM) is involved with the normal regulation of intraocular pressure (IOP) and dysregulation of ECM is part of the pathophysiology of an elevated IOP.  However, the regulatory pathways governing ECM homeostasis are unknown.  Matricellular proteins are associated with ECM regulation in other human tissues.  They were first to define the expression pattern, intracellular, and ultrastructural localization of SPARC, the prototypical matricellular protein, within the TM.  They were also first to demonstrate that SPARC-null mice have a lower IOP than their corresponding wild-type mice due to enhanced aqueous outflow.  They have shown that upregulation of SPARC increases IOP in perfused cadaveric human anterior segments with corresponding increases of fibronectin, laminin and specific collagens within the juxtacanalicular TM and TM cells.  These findings strongly implicate SPARC as having a pivotal regulatory role in the coordinated mechanisms governing ECM synthesis and accumulation. 

Publications