Harvard Ophthalmology Affiliates Receive $420,000 in Lions Grants for Eye Research

September 8, 2021

A key foundation partner to Harvard Ophthalmology, the Massachusetts Lions Eye Research Fund (MLERF) has selected several faculty to receive research awards. For academic year 2021-22, MLERF will provide $420,000 in funding to support innovative research projects across our affiliates.


Beetham Eye Institute at Joslin Diabetes Center ($105,000)

  • Mohamed Elmasry, MD, PhD, aims to determine the effect of integrating point-of-care macular spectral domain optical coherence tomography within a diabetic retinopathy ultrawide field retinal imaging telemedicine program. In addition to diabetic macular edema, Dr. Elmasry will evaluate and identify other macular pathologies such as age-related macular degeneration (AMD), epiretinal membrane, and pigment epithelial detachment that may affect vision in the populations of patients with diabetes.
  • Paolo S. Silva, MD, will evaluate whether retinal imaging data acquired using ultrawide field imaging combined with swept source optical coherence tomography cross-sectional imaging done both centrally and peripherally can better predict retinopathy severity and risk of vision loss than has been possible with current imaging modalities alone. These studies may find new markers of retinopathy progression and novel predictors of visual loss and provide the insight necessary to achieve more effective monitoring and treatment approaches.
  • Jennifer K. Sun, MD, MPH, and her team will evaluate the retinal microvasculature under conditions of normal versus increased oxygenation using adaptive optics scanning laser ophthalmoscopy and optical coherence tomography angiography imaging of the central microcirculation in eyes across the entire range of diabetic retinopathy severity. Longitudinal follow-up imaging of patients who have previously participated in MLERF-supported retinal imaging studies will allow the evaluation of the interactions between neural and vascular retinal tissues and their associations with visual function over time.

Boston Children's Hospital ($105,000)

  • Jing Chen, PhD, will study molecular factors of ocular birth defects caused by genetic mutations in WNT2B, a secreted signaling factor, that may affect embryonic organ development, specifically mammalian eye development. Earlier research using a mouse model found that photoreceptors are formed abnormally in these mice, with large clusters of photoreceptors arranged in wrong places in the eye. Dr. Chen and her team aim to further understand why this is occurring.
  • Eric Gaier, MD, PhD, aims to better understand the mechanism of suppression, a key driver of amblyopia development which also interferes with depth perception. Using a specially developed mouse model of suppression, Dr. Gaier will analyze different stimulus types and frequencies; examine brain activity during the suppression task through analysis of the signal recorded; and apply anti-suppression amblyopia therapy in an attempt to eliminate suppression and promote recovery.
  • Mary Whitman, MD, PhD, will investigate the role of interneurons in the development of nystagmus in albinism. Human nystagmus is indicated by vision-dependent development of the eye movement circuits in the first two months of life. Dr. Whitman and her team will examine the interneurons within the ocular motor nuclei throughout mouse development, both before and after eye opening, and compare between wildtype and albino mice.

Mass Eye and Ear ($105,000)

  • Elizabeth Rossin, MD, PhD, will conduct structure-based network analyses of genetic mutations that cause inherited retinal disorders (IRDs). Interpreting the results of genetic data to determine the cause of an IRD is currently a major challenge. The researchers are looking for a single causal mutation amongst a sea of benign genetic variation that exists within all human genomes. Dr. Rossin and her team hypothesize that one approach to tackle this problem is to analyze the 3-dimensional structure of proteins in their final biological form to better understand which mutations would cause IRDs.
  • David Wu, MD, PhD, will explore the role of retinal metabolism on early age-related macular degeneration (AMD). Recent work by Dr. Wu and others have found that photoreceptors, and the neighboring retinal pigment epithelial cells (RPE), share many metabolites, as part of their normal function. The RPE sits between the photoreceptors and the outer blood-retinal barrier (OBRB), and one of its functions is to support both the photoreceptors and the OBRB. Dr. Wu hypothesizes that if the photoreceptors were sick in some way, they might not share their usual metabolites with the RPE, changing RPE function and adversely affecting its maintenance role of the OBRB, which could lead to the deterioration that we see in AMD.  

Schepens Eye Research Institute of Mass Eye and Ear ($105,000)

  • Meredith Gregory-Ksander, PhD, will investigate how to restore microglia homeostasis as a treatment for glaucoma. Microglia are considered the resident immune cells of the retina and are responsible for normal maintenance of the retina. Chronic activation of microglia and the loss of their normal homeostatic/support function is thought to contribute to neurodegeneration by promoting harmful inflammation and in animal models of glaucoma, the extent of microglia activation correlates with the extent of retinal ganglion cell death and optic nerve degeneration. Dr. Gregory-Ksander and her team aim to determine if reducing microglia activation and promoting restoration of homeostasis will prevent progressive glaucoma.
  • Eric Ng, PhD, will work to determine the therapeutic potential of purified recombinant heparin-binding domain (HBD) protein in treating diabetic retinopathy. In previous research, recombinant HBD protein was found to potently inhibit vascular inflammation in the retina induced by vascular endothelial growth factor (VEGF) in a mouse model of retinal inflammation. The anti-inflammation effect of the recombinant HBD protein was dose-dependent and did not interfere with the beneficial functions of VEGF in neuroprotection and vascular homeostasis. Based on these findings, they hypothesized that recombinant HBD protein will specifically inhibit VEGF-mediated pathological vascular inflammation in diabetic retinopathy while allowing the beneficial functions of VEGF to maintain normal retinal function.
See also: Faculty, Grants, Research