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EYE DISEASES July 15-17, 2019 International Conference on EYE DISEASES July 15-17, 2019 Venue Sonesta Fort Lauderdale Beach 999 N Fort Lauderdale Beach Blvd Fort Lauderdale, FL Exhibitor Day-1 | Monday July 15, 2019 Keynote Talks Vascular Basement Membrane Thickening in Diabetic Retinopathy Sayon Roy Boston University School of Medicine, Boston, MA Biography Dr. Sayon Roy is a Professor of Medicine and Ophthalmology in Department Ophthalmology, Boston University. He completed his B.S. and M.S. from University of Kalyani, India. He received his PhD from Boston University. Dr. Roy’s seminal work has identified several genes in the retina that are abnormally expressed in diabetic retinopathy. His pioneering work has led to novel gene modulatory techniques in retinal vascular cells using antisense oligonucleotides via intravitreal injection. Dr. Roy has received numerous awards including the American Diabetes Association Research Award for the commitment and dedication towards the fight against diabetes, the 2006 Mentor of the Year Award from Boston University, and the 2008 Innovative Award from the Juvenile Diabetes Research Foundation Does Genomics Play a Role in Diabetic Retinopathy? Arup Das1, Sampath Kumar Rangasamy2, Finny Monickaraj1, David Duggan2, Nicholas Schork2 and Paul McGuire1 1University of New Mexico School of Medicine, Albuquerque, NM 2 Translational and Genomics Research Institute, NM Abstract Genetic risk factors play an important role in the development and progression of diabetic retinopathy (DR). Using a well- defined, clinical phenotype, we have examined the role of rare genetic variants in DR progression, or protection by undertaking whole exome sequencing (WES). We performed WES analysis on two cohorts of patients selected from Diabetic Retinopathy Genomics (DRGen) study population. Group 1 had “extreme” phenotype (No DR in spite of >25 years of diabetes) (n=6), while Group 2 had “advanced” DR (PDR within 15 years of diabetes) (n=6). DNA was isolated from white blood cells and the WES was performed using SureSelect All Human XT v5 exome kits, on Illumina NovaSeq platform. This was followed by an in-house downstream analysis pipeline to align sequence reads and complete variant calling and annotation. Analysis of rare coding variants using MAF cutoff revealed novel genetic variants with heterozygous missense mutations. Among the variants predicted to be disease-causing, variants in five genes (KLF17, COL18A1, CD33, PLEKHG5, ZNF395) with MAF<0.5% were enriched in the Group 2 (PDR), while variant in a gene (NKX2-3) with MAF<0.5% was shared among the cohort 1 (extreme phenotype). Thus, we identified coding sequence variants in a novel set of genes involved in the angiogenesis/ inflammatory pathway that contributes to DR progression, or protection. Future functional validation of the identified variants in disease pathogenesis could potentially lead to the identification of novel biomarkers and molecular targets for treating DR. Biography Dr. Arup Das is Regents’ Professor of Ophthalmology at University of New Mexico School of Medicine, Albuquerque, USA. After his medical education from Medical College of Calcutta, he did his PhD in Physiology at Medical College of Ohio, and then a postdoctoral fellowship in diabetic retinopathy research at Wayne State University in Detroit. Subsequently, he did his residency in Ophthalmology there, and then a retinal fellowship at Doheny Eye Institute, University of Southern California. Currently, Dr. Das maintains an active research lab funded by NIH and VA. His research interests include angiogenesis, retinal vascular biology, and genetics of diabetic retinopathy. Endothelial Progenitor Cells and Retinal Vascular Regeneration Alan W. Stitt Centre for Experimental Medicine, Queen’s University Belfast, Belfast, Northern Ireland, UK Abstract There is growing evidence that many vascular beds possess resident progenitor cells that have important roles in EYE-2019 | July 15-17, 2019 | Fort Lauderdale, FL 2 homeostasis and normal repair processes. In disease contexts, such as diabetes, these progenitors often become dysfunctional and this may make a significant contribution to the vasodegenerative pathology that is characteristic of many diabetic complications. This presentation will examine progenitor cell types with myeloid, mesenchymal or endothelial profiles and their role in regenerative medicine. The molecular profiles and mechanism of action of these progenitors will be discussed and examples shown of how exposure to the diabetic milieu can alter their vasoreparative function. Particular emphasis will be given to progenitors that regenerate damaged endothelium and a sub-type known as endothelial colony forming cells (ECFCs). Data will be shown that demonstrates how ECFCs have recently emerged as the principal endothelial progenitor both in vivo. The presentation will discuss the possibilities of treating vasodegenerative disease by harnessing vessel-resident regenerative cells and also using them for to regenerate ischaemic tissues. Biography Professor Stitt is the McCauley Chair of Experimental Ophthalmology with a research focus on pathogenesis and new therapeutic avenues for diabetic retinopathy and age-related retinal disease. He also contributes to the international academic community by serving on advisory boards, grant panels and as editor for Current Eye Research and Associate Editor for Diabetologia. He has received a Royal Society Merit Award, the Sir Jules Thorn Biomedical Science Award, and the 5th Fincham Medal. He is a member of the Royal Irish Academy (MRIA) and a Fellow of the Association for Research in Vision & Ophthalmology (FARVO). Diabetic Retinopathy: Mitochondria and a Web of Epigenetics Renu A. Kowluru Wayne State University, Detroit, MI Abstract In the pathogenesis of diabetic retinopathy, mitochondria are damaged in the retina and its vasculature, and the damaged mitochondria continues to fuel into the vicious cycle of free radicals. Mitochondrial dysfunction activates the apoptotic machinery and accelerated capillary cell apoptosis precedes the development of histopathology characteristic of diabetic retinopathy. Expression of many genes associated with mitochondrial homeostasis is also altered in diabetes. Recent evidence has clearly documented the role of epigenetics in gene expression, and diabetes is shown to alter the activities of many enzymes implicated in epigenetic modifications including DNA methylation and hydromethylation. This presentation will discuss how epigenetic modifications affect mitochondrial structural and genomic stability, and their role in the development of diabetic retinopathy. Biography Dr. Kowluru is a Professor and Director of Translational Research in the Ophthalmology and Visual and Anatomical Sciences Department at Wayne State University, Detroit. Her research is focused on understanding the molecular mechanism of diabetic retinopathy, especially the role of mitochondrial dysfunction and epigenetics. She has published over 160 peer- reviewed articles, and is on the editorial board of leading Vision and Diabetes journal. Dr. Kowluru serves as an expert reviewer on many NIH, Department of Defense and Veterans Administration panels. The research is currently funded by R01 awards from the National Eye Institute, and from a Private Foundation. The UPR Signaling in Bone Marrow Stem Cells and Diabetic Retinopathy Sarah X. Zhang Ira G. Ross Eye Institute, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, the State University of New York, NY Abstract Dysfunction of the bone marrow (BM)-derived angiogenic stem and progenitor cells is an important pathogenic factor contributing to the persistent vascular injury and degeneration in diabetic tissues. In this study, we investigate the role of unfolded protein response (UPR) signaling in diabetic BM stem cell dysfunction and their implication in diabetic retinopathy. In type 1 and type 2 diabetic mice, ER stress markers and inflammatory gene expression in BM mononuclear cells and hematopoietic progenitor cells increase dynamically with disease progression. Inhibition of ER stress by ex vivo or in vivo chemical chaperone treatment significantly improves the viability of BM stem cells and enhances their angiogenic function. ER stress inhibition also increases the number of circulating angiogenic cells, alleviates BM pathology, and promotes retinal vascular repair after ischemic injury in diabetic mice. Furthermore, manipulation of the UPR signaling mediated by the IRE/XBP1 or the CHOP pathways significantly altered bone marrow progenitor cell survival and function under normal and diabetic conditions. These findings suggest that targeting the UPR signaling in the BM and angiogenic stem cells may provide a novel and promising approach to the prevention and treatment for diabetic retinopathy. EYE-2019 | July 15-17, 2019 | Fort Lauderdale, FL 3 Plenary Session Activation of Classical Complement Pathway by Exosomes in Diabetic Retinopathy Julia Busik*, Chao Huang, Kiera Fisher, Sandra Hammer and Denis Proshlyakov Michigan State University, East Lansing, MI Abstract Diabetic retinopathy (DR) is a sight threatening microvascular complication of diabetes. Activation of complement system was recently implicated in the development of vascular damage and progression of DR. The mechanism(s) involved in complement system activation in DR are not fully understood. Exosomes, small vesicles that are secreted into the extracellular environment, have a cargo of complement proteins in plasma, suggesting
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