Joseph A. Bonanno
Joseph A. Bonanno, OD, PhD, FAAO, FARVO
Member, Berkeley Optometry Hall of Fame
Dr. Joseph A. Bonanno was born in Camden, New Jersey on October 12, 1953. He received his bachelor’s degree in biology from the University of Pennsylvania (1975), M.S. in Molecular Biology from UC Berkeley (1977), OD from UC Berkeley (1981), and PhD in Physiological Optics from UC Berkeley (1987). Dr. Bonanno joined the UC Berkeley School of Optometry faculty in 1989 and rose to Professor by 1997. In 1998, Dr. Bonanno joined the faculty at the Indiana University School of Optometry, became Associate Dean for Research in 2005, Associate Dean for Academic Affairs in 2007, and Dean in 2010. Dr. Bonanno will step down as Dean in June 2023.
Following the advice of his undergraduate advisor at Penn, Dr. Bonanno went west with visions of sunny warm beaches only to be engulfed in a cold fog while crossing the Golden Gate Bridge in August. He joined the UCB graduate program in Molecular Biology that was housed in the “Virus Lab” at Stanley Hall where he worked on Xenopus toad developmental biology with Professor John Gerhart. Sensing the need for something more practical, yet never having had an eye exam, he approached Dr. Darrell Carter in Minor Hall to find out about optometry.
During optometry school, Dr. Bonanno had the privilege to do a small research project with Berkeley Optometry Hall of Famers Ken Polse and Sheldon Miller on the stimuli of “corneal endothelial blebs” during contact lens wear. At the completion of the optometry program, Bonanno went back east to do a primary care residency at the Pennsylvania College of Optometry (1982) and then director of the contact lens service at Wills Eye Hospital, where he was one of the first two optometrists hired by Wills. Never having lost the research interest, he returned to Berkeley to work with Ken Polse on the physiological effects of contact lens wear. In Professor Polse’s lab, he developed a non-invasive method for measuring changes in corneal stromal acidity in humans wearing contact lenses. This was verification that corneal pH decreases during lens wear due to hypoxia and increased carbon dioxide and provided an explanation for the formation of transient endothelial blebs.
To broaden the research experience, Dr. Bonanno received an F32 NIH postdoctoral fellowship in 1987. He did a project at the LSU department of ophthalmology with Professor Steve Klyce where he determined the mechanism for chloride uptake in corneal epithelial cells that is necessary for fluid transport to the tears when stimulated by the sympathetic nervous system. Following this work on epithelium, Bonanno returned to Berkeley to work with Professor Terry Machen in the department of physiology-anatomy. There he learned the use of fluorescent probe technology which laid the groundwork for many years studying pH regulation and ion transport in the corneal endothelium.
In 1989, Dr. Bonanno joined the faculty at Berkeley Optometry. His lab focused on: 1) determining the mechanism of the corneal endothelial pump and 2) measuring contact lens oxygen delivery. In the first project, the working hypothesis was that the endothelium secreted bicarbonate that drove water flux osmotically keeping the stromal hydration constant. After more than a decade of work the research indicated that the endothelial pump did not secrete bicarbonate. A new hypothesis of absorption of lactic acid-linked water flux was developed. Subsequent endothelial dystrophy models were consistent with this model. This work was funded by the National Eye Institute for 29 years. In the second project, Dr. Bonanno’s interest in contact lens oxygen delivery led him to develop a non-invasive method for measuring tear oxygen levels under rigid lenses in rabbits, which was later extended to human subjects wearing standard hydrogels and silicone-hydrogels. This was funded by an NEI grant and contact lens manufacturers. More recent research has examined the function of the membrane proton transporter SLC4A11, which is defective in Congenital Hereditary Endothelial Dystrophy. Dr. Bonanno’s lab discovered that SLC4A11 is an ammonia-activated mitochondrial uncoupler. The function of SLC4A11 is to limit oxidative stress in corneal endothelial cells, preventing cell death when catabolizing the amino acid glutamine. This project is currently funded by the NEI.
Dr. Bonanno has authored or co-authored more than 110 peer-reviewed articles and gave numerous invited lectures. Dr. Bonanno was a member of the National Advisory Eye Council (NIH) and served on several AAO and ARVO committees. Dr. Bonanno is a Garland Clay (1994) and a Glenn Fry Awardee (2000).