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M. Elizabeth Fini, PhD seeks novel genetic targets for treating glaucoma
M. Elizabeth Fini, PhD seeks novel genetic targets for treating glaucoma

Each year the Glaucoma Research Foundation awards Shaffer Grants to worthy investigators with innovative ideas.

A clear research focus and strong leadership from an expert board of Scientific Advisors is key to the success of our Shaffer Grants for Innovative Glaucoma Research.

Some of the most important discoveries in scientific research come from an investigator with a new, untested idea who needs funding to explore a creative project. Shaffer Grants provide seed money for pilot research projects that hold promise and explore new ideas.

Following are annual research grants awarded in recent years. All of our grants to explore new ideas are in the amount of $40,000.

The 2016 Frank Stein and Paul S. May Grants for Innovative Glaucoma Research


David T. Stark, MD, PhD
Stein Eye Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA
Project: Endocannabinoids in Retinal Ganglion Cell Regeneration

Download Dr. Stark's final project research poster (PDF) »

Final Report Summary: Many optic nerve diseases result in permanent loss of vision. This occurs in part because the intrinsic growth capacity of retinal ganglion cells rapidly declines after birth, and injured central nervous system axons fail to regenerate. The scientific community has learned a great deal about molecular signals that can support regeneration of damaged neural connections, but there is an urgent need to identify as many pro-regenerative signals as possible because it is not clear which of these might actually translate to use in patients.

Generous support from the Glaucoma Research Foundation allowed us to develop a strategy to comprehensively assess an entire class of biomolecules called lipids for differences that occur during optic nerve regeneration. We hope to use this approach to identify candidate molecules that might represent previously unknown pro-growth signals.


Frank Talke, PhD
University of California, San Diego
Project: Development of an Optical-based Intraocular Pressure Sensor

Download Dr. Talke's final project research poster (PDF) »

Final Report Summary: We have developed an intraocular pressure sensor based on the principle of interferometry. The sensor is comprised of a diaphragm and a glass substrate. By directing monochromatic light towards the active sensing region and applying pressure, one can observe interference fringes as the diaphragm deflects. Using the principle of interferometry, we were able to back calculate pressure using the images captured by a camera. From our studies, we have found the best results using silicon nitride as the diaphragm material. The sensor read-out can be further optimized by coating a thin layer of silicon nitride onto the glass substrate. In order to further demonstrate proof of concept, our sensor was also tested ex-vivo using a rabbit eye model. Thus far, we have achieved 0.8 mmHg resolution. Our results show that the sensor response is repeatable and agree with mathematical models.

The 2016 Shaffer Grants for Innovative Glaucoma Research


Kevin Park, PhD
University of Miami Miller School of Medicine, Miami, FL
Funded by The Melza M. and Frank Theodore Barr Foundation, Inc.
Project: Axon-astroglial Interaction and its Effects on Optic Nerve Repair

Download Dr. Park's final project research poster (PDF) »

In glaucoma, the optic nerve which sends visual information from eye to brain gets damaged. Once damaged, the optic nerve does not regrow back to the brain, resulting in permanent blindness. Therefore, to restore visual function in glaucoma patients, it might be necessary to promote injured optic nerves to regenerate and reconnect to their original targets.

In the last several years, researchers have identified gene therapies that can promote optic nerve regeneration. However, there is a still major problem. Optic nerves are mostly incapable of growing straight back to the brain, and often fail to reach the brain. In our research, we seek to understand the cellular and genetic factors that prevent these nerves to correctly find their targets. Towards this goal, we first discovered that optic nerves regenerate physically on the surface of astrocytes which are the support cells in the optic nerve. Therefore, we reveal that optic nerve regeneration and navigation are in fact shaped by astrocytes.

Second, we discovered that certain genes, namely Ncad expressed in the astrocytes, are important for optic nerve interaction with astrocytes, and for optic nerve regeneration. Our study identified the key cellular and genetic players that shape optic nerve regeneration and navigation. Ultimately, our research will help elucidate factors that prevent proper optic nerve regeneration and guidance, and to find strategies that promote reconnection of damaged optic nerves and restore visual functions following optic nerve damage.


Ian Pitha, MD, PhD
Johns Hopkins University, Wilmer Eye Institute, Baltimore, MD
Funded by Dr. James and Elizabeth Wise
Project: Neuroprotection through Altered Scleral Biomechanics

Download Dr. Pitha's final project research poster (PDF) »

Final Report Summary: To date, the only way to stop vision loss from glaucoma is intraocular pressure (IOP) reduction by daily medication use, laser procedure, or incisional surgery. In some patients IOP reduction is difficult to accomplish or glaucomatous vision loss occurs despite substantial IOP reduction.

These clinical situations highlight the need for development of IOP-independent, glaucoma treatment strategies otherwise known as neuroprotection. One promising neuroprotective therapeutic for glaucoma treatment is the blood pressure medication losartan. Losartan’s protective activity is due to prevention of remodeling processes that occur in the wall of the eye (the sclera) during glaucoma.

In these studies we have shown that losartan treatment targets specific cells within the sclera called fibroblasts. Fibroblasts exposed to losartan are prevented from becoming “activated” and remodeling the scleral tissue. In addition, we have developed long-lasting, drug releasing microparticles to prevent scleral remodeling in glaucoma.


Carla J. Siegfried, MD
Washington University School of Medicine, St. Louis, MO
Funded by The Alcon Foundation
Project: Pathological Alterations in the Trabecular Meshwork Following Vitrectomy and Lens Extraction: A Model of Oxidative Stress

Download Dr. Siegfried's final project research poster (PDF) »

Final Report Summary: Elevation of pressure in the eye is the only risk factor for glaucoma that can be modified. Improved understanding of how the eye’s natural drain is damaged can provide insights to new treatments and prevention of this blinding condition.

We have measured oxygen levels inside the eyes of patients undergoing eye surgery with a small probe and found increased oxygen levels in patients who have had removal of the gel in the back of the eye, a procedure performed for various retinal diseases. Patients who have had this procedure nearly always require cataract surgery and this combination of procedures lead to an increased risk of glaucoma. This excess oxygen may be the source of molecules that cause damage to the cells of the natural drain of the eye. In addition, the level of antioxidants, compounds that protect the cells from this damage, are decreased following this combination of surgeries.

By performing these two procedures (removal of gel and then lens removal), we predicted increased oxygen levels in the front of the eye in the area of the natural drain in a glaucoma model. We were unable to duplicate these findings in this model, but did enhance our techniques utilizing a laser to dissect these specific cells in the drain of the eye to study changes associated with damage and then study the how these cells may have altered programming of their genetic code. In this manner, we can now learn more precisely how these cells are damaged and potentially identify patients who are at risk for damage and new ways to treat glaucoma.


W. Daniel Stamer, PhD
Duke University Eye Center, Durham, NC
Funded by The Alcon Foundation
Project: Role of Exosomes in Glaucomatous Lamina Cribrosa Remodeling

Final Report Summary: In this project we have optimized techniques to isolate and characterize exosomes from lamina cribrosa cells. Exosomes are small vesicles that are released by cells to perform a variety of functions. In the lamina cribrosa, like the trabecular meshwork we hypothesize that exosomes participate in the turnover of extracellular matrix and homeostatic signaling with cell neighbors, particularly in response to elevations in intraocular pressure/pulsations. In the present study we mimicked pressure pulsations by cyclically stretching lamina cribrosa cells and collecting/purifying released exosomes from the cell culture media. We observed that exosomes from glaucomatous lamina cribrosa cells were different than exosomes from normal cells. These differences hold the potential to provide information about abnormal remodeling of the optic nerve head in early stages of glaucoma.


Evan B. Stubbs, Jr., PhD
Edward Hines, Jr. VA Hospital, Hines, IL
Funded by The Alcon Foundation
Project: Mitochondrial-specific Antioxidant XJB-3-151 as a Novel Therapeutic Strategy to Lower Elevated Intraocular Pressure

Download Dr. Stubbs' final project research poster [1 of 2] (PDF) »

Download Dr. Stubbs' final project research poster [2 of 2] (PDF) »

Final Report Summary: Glaucoma is a silent disease that, over time, kills the nerve cells of the retina leading to irreversible blindness. Current treatment options are restricted to non-specific interventions aimed at lowering intraocular pressure (IOP). For many glaucomatous patients, however, pharmacological and surgical management of IOP does not always help. The development of targeted therapeutic strategies directed at the cause of elevated IOP is critical for the advanced management of glaucoma. The cause of elevated IOP most likely involves a molecule called transforming growth factor-β2 (TGF-β2). Funding support from the Glaucoma Research Foundation Shaffer Grant has allowed our lab to advance our understanding of exactly how TGF-β2, a multifunctional cytokine, promotes increases in IOP of patients with POAG. We found that specific cells in the eye, called TM cells, constitutively express and secrete TGF-β2, highlighting the TM as a viable targetable source of TGF-β2. This molecule was further found to elicit harmful and pronounced oxidative stress to the TM. Our findings are consistent with other studies also reporting elevated levels of oxidative stress markers in the eyes of POAG patients, along with altered expression of antioxidant defenses in the TM. Results from this Shaffer Grant study also show that targeting antioxidants such as XJB-5-131 to the TM significantly attenuates expression and release of TGF-β2 from cultured human TM cells. Of equal importance, XJB-5-131 protected human primary TM cells against TGF-β2 mediated changes in expression of specific extracellular matrix proteins. These exciting findings are being put to the challenge to see if targeting antioxidants to the TM in porcine and human eyes will lower IOP. To do this, we have encapsulated small beads, called nanoparticles, with various test agents. We are seeing, for the first time, that these nanoparticles can markedly reduce IOP by reducing endogenous expression of TGF-β2. Collectively, our findings support targeted disruption of constitutive TGF-β2 expression within the eye using antioxidant-encapsulating nanoparticles and raises enthusiasm that this strategy will be a clinically useful and effective new therapy by which to better manage IOP in patients with POAG.


David A. Sullivan, MS, PhD, FARVO
Co-investigator: Louis R. Pasquale, MD
Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA
Dr. Henry A. Sutro Family Grant for Research
Project: Estrogen & Glaucoma

Download Dr. Sullivan's final project research poster (PDF) »

Final Report Summary: Glaucoma is characterized by a gradual loss of retinal ganglion cells (RGCs), which leads to a loss of vision. The most common form of glaucoma, occurring in 70 to 90% of patients, is primary open angle glaucoma (POAG).

One of the most compelling epidemiological features of POAG is that its incidence shows a striking sex-related difference. Women have a significantly lower incidence of POAG, as compared to men, until the age of 80 years. This sex-related difference has been linked to the extent of lifetime estrogen exposure. Indeed, there is a strong assocation between increased estrogen exposure and a reduced POAG risk. Conversely, studies have shown that a decreased exposure (i.e. early loss of estrogens), confers an increased risk of POAG. We hypothesize that an early estrogen deficiency accelerates the aging of the optic nerve and predisposes this nerve to glaucomatous damage.

To test our hypothesis we determined whether early estrogen deficiency is associated with heightened intraocular pressure, RGC loss and glaucoma in an animal model. Our results demonstrate that estrogen deprivation does promote the development of glaucoma in female mice. To continue these studies, we seek to determine whether estrogen administration will serve as a novel preventive treatment for glaucoma, and in particular, POAG. If so, our research will have significantly advanced our understanding of the role of estrogen in the pathophysiology of glaucoma.

The 2015 Frank Stein and Paul S. May Grants for Innovative Glaucoma Research

Paul L. Kaufman, MD
University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin
Co-funded by The Alcon Foundation
Project: Gene Therapy for Glaucoma

Matthew A. Smith, PhD
University of Pittsburgh, Pittsburgh, PA
Project: Measuring the In-vivo Effects on the Optic Nerve Head of Acute Variations in Cerebrospinal Fluid Pressure


Gülgün Tezel, MD
Columbia University, New York, NY
Project: Molecular Biomarkers of Glaucoma

In September 2015, IOVS (vol. 56 no. 10) published results from this research project in "Proteomics Analysis of Molecular Risk Factors in the Ocular Hypertensive Human Retina." The published paper concluded that" "molecular alterations detected in the ocular hypertensive human retina as opposed to previously detected alterations in human donor retinas with clinically manifest glaucoma suggest that proteome alterations determine the individual threshold to tolerate the ocular hypertension-induced tissue stress or convert to glaucomatous neurodegeneration when intrinsic adaptive/protective responses are overwhelmed."

The 2015 Shaffer Grants for Innovative Glaucoma Research

Donald L. Budenz, MD, MPH
University of North Carolina, Chapel Hill, NC
Dr. Henry A. Sutro Family Grant for Research
Project: Incidence of Glaucoma and Glaucoma Progression in an Urban West African Population

Richard T. Libby, PhD
University of Rochester Medical School, Rochester, NY
Funded by The Alcon Foundation
Project: Understanding Axonal Degeneration Pathways in Glaucoma

Paloma Liton, PhD
Duke University Eye Center, Durham, NC
Funded by Dr. James and Elizabeth Wise
Project: Lysosomal Enzymes, Glycosaminoglycans and Outflow Pathway Physiology

Lyne Racette, PhD
Indiana University, Indianapolis, IN
The Dr. Miriam Yelsky Memorial Research Grant
Project: Early Detection of Glaucoma Progression using Structural and Functional Data Jointly

Shandiz Tehrani, MD, PhD
Oregon Health & Science University, Portland, OR
Funded by The Alcon Foundation
Project: Local Drug Delivery to the Optic Nerve Head as a Novel Treatment in Experimental Glaucoma

The 2014 Shaffer Grants for Innovative Glaucoma Research


Jeff M. Gidday, PhD
Washington University School of Medicine, St. Louis, Missouri
The Dr. Miriam Yelsky Memorial Research Grant
Project: Delayed Post-Conditioning for Glaucoma Neuroprotection

Vikas Gulati, MD
Truhlsen Eye Institute, University of Nebraska Medical Center, Omaha, Nebraska
Funding provided by a grant from The Alcon Foundation
Project: Effect of Vascular Endothelial Growth Factor Blockers on Aqueous Humor Dynamics

David Krizaj, PhD
Moran Eye Institute, University of Utah, Salt lake City, Utah
Funding provided by Dr. James and Elizabeth Wise
Project: RGC Mechanotransduction as a Target in Glaucoma


Dr. Liu in the lab

Yutao Liu, MD, PhD
Medical College of Georgia, Georgia Regents University, Augusta, Georgia
Funding provided by a grant from The Alcon Foundation

Project: Exosomal RNAs and Aqueous Humor Dynamics

Dr. Liu's research results were published in an article titled "Human Aqueous Humor Exosomes" in the January 18, 2015 edition of the peer-reviewed journal Experimental Eye Research.

Stuart J. McKinnon, MD, PhD
Duke University Medical Center, Durham, North Carolina
Funding provided by Dr. James and Elizabeth Wise

Project: Neuroinflammation: The Role of Lymphocytes in Glaucoma

For his research project to determine whether therapies can be designed to modulate the immune system to prevent vision loss and blindness in glaucoma patients, Stuart J. McKinnon, MD, PhD was awarded the 2016 Shaffer Prize for Innovative Glaucoma Research. The Shaffer Prize, presented annually by Glaucoma Research Foundation, recognizes a researcher whose project best exemplifies the pursuit of innovative ideas in the quest to better understand glaucoma.

Robert W. Nickells, PhD
University of Wisconsin, Madison, Wisconsin
Dr. Henry A. Sutro Family Grant for Research
Project: Purinergic Signaling of Neuroinflammatory Glial Responses in a Model of Optic Nerve Damage

Colm O’Brien, MD, FRCS
Mater Misericordiae University Hospital, Dublin, Ireland
Funding provided by a grant from The Alcon Foundation
Project: Caveolins, Calcium Signalling and Fibrosis of Lamina Cribrosa Cells in Glaucoma

Joshua D. Stein, MD, MS
W.K. Kellogg Eye Center, University of Michigan, Ann Arbor, Michigan
Funding provided by the Glaucoma Research Foundation Board of Directors
Project: A Dynamic, Personalized Glaucoma Monitoring Decision Support Tool

2013 Frank Stein and Paul S. May Grants for Innovative Glaucoma Research


John H. Fingert, MD, PhD
University of Iowa, Department of Ophthalmology and Visual Sciences, Iowa City, Iowa

Project: Molecular Genetic Study of Normal Tension Glaucoma using Transgenic Mice

In February 2015, Ophthalmology Times reported that Dr. Fingert's continuing research provides strong evidence that mutation of the TBK1 gene can lead to glaucoma and may provide insights into disease mechanisms and future treatments. “Hopefully this will open up a new field for low-pressure glaucoma research and treatment,” Dr. Fingert said. He presented his research results at the 2014 meeting of American Academy of Ophthalmology.


Yvonne Ou, MD
University of California San Francisco, Department of Ophthalmology, San Francisco, California

Project: Investigating Axonal Death Pathways in Glaucoma

"Our goal was to investigate the parts of the optic nerve cell, specifically axons and synapses, which may be vulnerable early in the course of the disease."

David Sretavan, MD, PhD
University of California San Francisco, San Francisco, California

Project: Pathophysiological Progression in Single RGC Axons Following Microscale Compressive Injury

2013 Shaffer Grants for Innovative Glaucoma Research

Anneke I. den Hollander, PhD
Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
The 2013 Dr. Miriam Yelsky Memorial Research Grant

Project: Dissecting the Genetic Causes of Congenital and Juvenile Glaucoma


M. Elizabeth Fini, PhD
University of Southern California, Institute for Genetic Medicine, Los Angeles, California
Funding provided by a grant from the Merck Department of Continuing Education

Project: Novel Mucins and Aqueous Outflow

Recent studies suggest that the glycocalyx in the outflow pathways of the eye may be much more extensive than previously imagined. The idea that mucins might be present in this lining layer and play a role in ocular hypertension has not been previously considered. If confirmed, the findings will open a new line of research that could ultimately lead to significant innovation, as drugs that control amounts of the novel mucins or that target specific glycosylating enzymes could lead to a new treatment paradigm for glaucoma.


Andras M. Komaromy, DrMedVet, PhD
Michigan State University, East Lansing, Michigan
Funding provided by a grant from The Alcon Foundation

Project: Gene Therapy in a Spontaneous Canine Model of Primary Open-Angle Glaucoma

For his research on the potential of gene therapy to provide lasting control of intraocular pressure in glaucoma patients with known genetic defects, András Komáromy, DVM, PhD was awarded the 2015 Shaffer Prize for Innovative Glaucoma Research. The Shaffer Prize, presented annually by the GRF Scientific Advisory Committee, recognizes a researcher whose project best exemplifies the pursuit of innovative ideas in the quest to better understand glaucoma. Dr. Komáromy studies the molecular causes of inherited eye diseases in dogs and is working to develop gene therapies to stop vision loss. By identifying and treating gene mutations in dogs, his research moves us closer to gene therapy that could one day be used to manage and prevent glaucoma in humans.

Colleen M. McDowell, PhD
University of North Texas Health Science Center, Fort Worth, Texas
Funding provided by a grant from The Alcon Foundation

Project: Retina Ganglion Cell Subtype Specific Cell Death in a Mouse Model of Human Primary Open-Angle Glaucoma

Lin Wang, MD, PhD
Devers Eye Institute/Legacy Research Institute, Portland, Oregon
Funding provided by a grant from The Alcon Foundation

Project: Noninvasive Assessment of Dynamic Autoregulation in Optic Nerve Head

2012 Frank Stein and Paul S. May Grants for Innovative Glaucoma Research

Leonard A. Levin, MD, PhD, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin

Project: Sustained-Release Formulations of Redox-Active Drugs for Neuroprotection in Glaucoma


Alexander C. Theos, PhD, Georgetown University, Washington, D.C.

Project: GPNMB Deficiency and Associated Cytotoxicity in Pigment Dispersion Syndrome, a Precursor of Pigmentary Glaucoma

Dr. Theos' research results were published in an article titled "PKD Domains Distinguish PMEL and GPNMB Localization" in a 2013 edition of the peer-reviewed journal Pigment Cell & Melanoma Research. "This work would not have been completed without the support of the Glaucoma Research Foundation," Dr. Theos said.


Derek S. Welsbie, MD, PhD, The Johns Hopkins University School of Medicine, Baltimore, Maryland

Project: Evaluating the Role of the c-Jun N-terminal Kinase Cascade in Retinal Ganglion Cell Death

Dr. Welsbie's research results were published in an article titled "Functional genomic screening identifies dual leucine zipper kinase as a key mediator of retinal ganglion cell death" in the March 5, 2013 edition of the peer-reviewed journal PNAS (Proceedings of the National Academy of Sciences).

Dr. Welsbie was awarded the 2014 Shaffer Prize for Innovative Glaucoma Research by the Glaucoma Research Foundation. The Shaffer Prize recognizes the researcher whose project, funded by a Shaffer Grant in a given year, best exemplifies the pursuit of innovative ideas in the quest to better understand glaucoma.

2012 Shaffer Grants for Innovative Glaucoma Research

David Andrew Feldheim, PhD, University of California Santa Cruz, Santa Cruz, California

Project: Transcriptional Control of RGC Health and Function

Purushottam Jha, PhD, University of Arkansas for Medical Sciences, Little Rock, Arkansas

Project: Complement System as Therapeutic Target for Glaucoma


Melanie Kelly, PhD, Dalhousie University, Halifax, Nova Scotia, Canada

Project: Manipulating Lipid Signaling to Treat Glaucoma and Ocular Disease

Dr. Kelly reports: "Our research was able to accomplish all of the aims for this project." Her laboratory's findings were published in the April 11, 2103 issue of the journal Neuropharmacology (Slusar et al., 2013)

Wei Li, PhD, University of Miami School of Medicine, Miami, Florida

Project: Global Mapping of Glaucoma Autoantibody Biomarkers

Rachel Wong, PhD, University of Washington, Seattle, Washington

Project: Exploring Loss and Recovery of Visual Receptive Field Properties in Populations of Retinal Ganglion Cells in a Glaucoma Model

2011 Frank Stein and Paul S. May Grants for Innovative Glaucoma Research


William H. Baldridge, PhD, Dalhousie University, Halifax, NS Canada

Project: Calcium-permeable AMPA Receptors and Retinal Ganglion Cell Death during Glaucoma

"This study investigated the D-serine modulation of non-NMDA ionotropic glutamate receptors expressed by inner retinal neurons. To our knowledge, this is the first study to address specifically the effect of D-serine on AMPA ⁄ kainate receptors in intact central nervous system tissue, to identify its effect on calcium permeable AMPA receptors and to report the endogenous inhibition of AMPA ⁄ kainate receptors." - from the abstract of Dr. Baldridge's paper published in volume 35 of the European Journal of Neuroscience, 2012.

Hani Levkovitch-Verbin, MD, MPA, Goldschleger Eye Institute, Tel Hashomer, Israel

Project: Age-related Increased Vulnerability of Retinal Ganglion Cells to Elevated IOP- Mechanism and Neuroprotection.

Keith R. Martin, PhD, Cambridge Centre for Brain Repair, Cambridge, United Kingdom

Project: Pre-clinical Assessment of Human Retinal Ganglion Cell Neuroprotection by Human Stem Cells: Efficacy and Mechanism.

2011 Shaffer Grants for Innovative Glaucoma Research

Eduardo J. Chichilnisky, PhD, The Salk Institute, La Jolla, CA

Project: Physiological Changes and Loss of Distinct Ganglion Cell Types in Glaucoma


Gareth R. Howell, PhD, The Jackson Laboratory, Bar Harbor, ME

Project: Understanding the Mechanisms of Wlds-mediated Protection in Glaucoma

Dr. Gareth Howell was awarded the 2013 Shaffer Prize for Innovative Glaucoma Research for his study investigating the mechanism by which a spontaneous mutation (Wallerian degeneration slow, Wlds) prevents retinal ganglion cell death in glaucoma. The Shaffer Prize recognizes the researcher whose project, funded by a Shaffer Grant in a given year, best exemplifies the pursuit of innovative ideas in the quest to better understand glaucoma.


Janice Vranka, PhD, Oregon Health & Science University, Portland, Oregon

Project: Versican as Primary Contributor to Aqueous Humor Outflow Resistance

Dr. Vranka’s project studied Versican, a large proteoglycan that is known to interact with many other proteins also present in the trabecular meshwork, which is thought to be the primary contributor to outflow resistance. Understanding of the overall structure and organization of the outflow resistance, which directly affects the intraocular pressure system will help to enable the development of better treatments to reduce pressure for primary open-angle glaucoma patients. Dr. Vranka’s findings were published in the July 2011 issue of Investigative Ophthalmology & Visual Science (IOVS).

Shunbin Xu, MD, PhD, Rush University Medical Center, Chicago, Illinois

Project: MicroRNAs in Retinal Ganglion Cells and Glaucomatous Neurodegeneration.

2010 Shaffer Grants

Emmanuel Buys, PhD, Massachusetts General Hospital, Boston, Mass.

Project: Soluble guanylate cyclase alpha 1-deficient mice: a novel murine model of elevated IOP and glaucoma


Tonia S. Rex, PhD, University of Tennessee Health Science Center, Memphis, Tenn.

Project: Systemic Delivery of a Neuroprotective Agent to Protect against Glaucomatous Cell Death in the DBA2/J Mouse

Dr. Rex was awarded the 2012 Shaffer Prize for Innovative Glaucoma Research for her research investigating the effectiveness of a neuroprotective therapy in a model of inherited glaucoma. Dr. Rex used gene delivery to provide long-term production of a modified form of erythropoietin (EPO), a hormone that induces red blood cell production but is also a neuroprotective cytokine. Gene delivery is ideal for glaucoma since it is a slowly progressing retinal degenerative disease. The Rex lab used the DBA/2J mouse model of pigment dispersion glaucoma. They treated prior to the onset of cell death, then monitored intraocular pressure and counted the number of surviving retinal ganglion cells.


Yi Zhao, PhD, Ohio State University, Columbus, Ohio

Project: Nanoengineered In Vitro Trabecular Meshwork ™ Model for Systematic Investigation of Aqueous Humor Outflow Resistance

This project developed an in vitro model using 3D porous polymer for studying the aqueous humor outflow in the eye. The results show that the in vitro model is a useful alternative to human donors because it allows parallel screening of a wide array of potent parameters that may regulate intraocular pressure. It provides a promising solution for unveiling the underlying mechanism of primary open-angle glaucoma and exploring effective therapeutics. Several proceeding papers and abstracts were published in conferences related to eye research and biomedical micro/nanotechnology, including the journals Biomedical Microdevices and Annals of Biomedical Engineering.


An Zhou, PhD, Robert S. Dow Neurobiology Laboratories, Portland, Oregon

Project: Epigenetic regulation of HIOP-induced endogenous neuroprotection in rat retinas

“In this GRF-supported study, we treated retinas with three related but different, high IOP-induced ischemic conditions: preconditioning (short ischemia, causing litter injury), injurious (prolonged ischemia, severe injury), and tolerant (preconditioning followed by prolonged ischemia, protected from injury). For retinas prepared from these three experimental conditions, we performed proteomic analyses using the latest technology so that proteins that are uniquely regulated under each condition can be identified. We then performed neuroanatomical analyses to validate proteomic findings and analyzed additional proteins that were suggested by proteomic findings. As a result, we report that, in ischemic-injured or ischemic-tolerant retinas, there is a striking difference in the abundance of a number of proteins that we know play important roles in neuroprotection against ischemic injury in brain. These proteins, if their roles in neuroprotection in the retina are fully established in the future by more comprehensive studies, may present novel therapeutic targets in treating retinal disorders including glaucomatous conditions.” Dr. Zhou's findings were published in the International Journal of Physiology, Pathophysiology and Pharmacology.

2009 Shaffer Grants


Haiyan Gong, MD, PhD, Boston University School of Medicine, Boston, Mass.

Project: A Study of the Dynamics of Schlemm's Canal Endothelial Cells using a Three-dimensional Cell Culture Device with Real-time Imaging. (Pictured: Dr. Gong examines samples using an electron Microscope).

"Schlemm's canal endothelial cells are believed to be one of the resistance sites crossed by the aqueous humor before entering the blood circulation and are likely to play an important role in the regulation of aqueous humor outflow resistance. In this study, we modified and applied a three-dimensional (3D) cell culture device which was recently developed at MIT to study the dynamics of Schlemm's canal endothelial cells. Our results demonstrated that our 3D cell culture device enables a real-time imaging of giant vacuole formation and tracers crossing the cultured endothelial cell monolayer in a controlled experimental condition. We showed that using a chemical, which can induce the cell into a more relaxed state, can promote giant vacuole formation. This result translates to an increase in drainage of aqueous humor and a decrease in pressure within the eye, similar to results established in animal models. This finding further validates our 3D cell culture devices as an experimental model for future glaucoma studies."


Deborah C. Otteson, PhD, University of Houston College of Optometry, Houston, Texas

Project: The Role of DNA Methylation in Regulating Eph Receptor Expression in the Retina

Dr. Otteson studied how retinal ganglion cells turn on and off the genes that regulate the normal patterns of connections during optic nerve development. Her overall aim was to enhance the development of regenerative therapies to restore the optic nerve and vision in glaucoma patients. She published the results of her findings in the September, 2010 edition of the journal Vision Research.

2008 Shaffer Grants

Paul Habib Artes, PhD, Dalhousie University, Halifax, NS, Canada

Project: Analysis of Progression in Glaucoma

Jamie Craig, PhD, Flinders University of South Australia

Project: Genome-wide Association in Primary Open Angle Glaucoma: The Blindness in Glaucoma Genetic Epidemiology Relative Risk Study

Brad Fortune, OD, PhD, Devers Eye Institute, Portland, Oregon

Project: Imaging the Course of Axonal Degeneration in Experimental Glaucoma


Kate E. Keller, PhD, Casey Eye Institute, Portland, Oregon

Project: RNAi Gene Silencing of Enzymes in the Glycosaminoglycan Biosynthetic Pathway

Dr. Keller was awarded the 2010 Shaffer Prize for Innovative Glaucoma Research for her research investigating the role of Glycosaminoglycans (GAGs) in fluid outflow resistance in the trabecular meshwork of the eye. Experimental results from this study could potentially lead to new therapies for lowering eye pressure in patients with primary open-angle glaucoma. Dr. Keller published her results in the scientific journals Investigative Ophthalmology and Visual Science and Experimental Eye Research.

Raquel L. Lieberman, PhD, Georgia Institute of Technology, Atlanta, Georgia

Project: Development of Pharmacological Chaperone Therapy for Inherited Primary and Juvenile Open Angle Glaucoma


Yutao Liu, MD, PhD, Duke University Medical Center, Durham, North Carolina

Project: Investigation of Gene Copy Number Variants in Primary Open Angle Glaucoma

"Thanks very much for your support of my research project in 2008. Your funding support initiated my CNV research program in POAG. With your funding, I then obtained further research funding from Duke Translational Research Institute in 2009 and American Health Assistance Foundation in 2010. Now I have published my research in PLoS ONE journal. Our work is the first to establish the potential connection between Krabbe disease and POAG. We found that GALC deletion could contribute approximately 1% of POAG cases. The GALC deletion carrier has 3-5 times more risk than a non-carrier."

For information about grants awarded prior to 2008, please contact the Glaucoma Research Foundation at (415) 986-3162.

Last reviewed on January 11, 2018

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