Dr. Sayon Roy

Professor

Education:

Ph.D. Boston University
Post-doctoral fellowship Harvard Medical School, Harvard University

General field of research:

Diabetic Microvascular Complications

Affiliations other than medicine:

Evans Center for Interdisciplinary Biomedical Research
Department of Ophthalmology

Contact information:

Office
650 Albany Street
Phone: 617-638-4110

sayon@bu.edu

Research group information

Amanda Tang, Medical Student, ahtang@bu.edu
Andre Pinheiro, Post-doctoral Fellow, andrepip@gmail.com
Argyrios Chronopoulos, Post-doctoral Fellow, aris@bu.edu
Ashley Pysczynski, Undergraduate Student, ashpski@gmail.com
Colleen Moore, Medical Student, Colleen.Moore@umassmed.edu
Ethan Tseng, Undergraduate Student, ethant@bu.edu
John Ha, Graduate Student, johnha1@gmail.com
Julia Manasson, Medical Student, manasson@bu.edu
Kyle Trudeau, Undergraduate Student, kmtru@bu.edu
Melissa Wong, Medical Student, mmywong@bu.edu
Michael Bobbie, Undergraduate Student, mwbobbie@bu.edu
Sumon Roy, Graduate Student, srchewie@bu.edu
Yugal Behl, Post-doctoral Fellow, ybehl@bu.edu

Keywords:

Diabetic retinopathy, Gene therapy, Vascular basement membrane thickening, Gap junction intercellular communication, Animal/primate model of diabetes, Extracellular matrix and diseases

Summary of research interest:

We are working on several projects related to the pathogenesis of diabetic microangiopathy, in particular, diabetic retinopathy. One of the projects involves applying a novel gene therapeutic strategy to normalize altered gene expression in the retinal capillary cells with the goal of preventing characteristic lesions of diabetic retinopathy.

A second project, aims at understanding the role of gap junction intercellular communication in the development of retinal vascular lesions associated with diabetic retinopathy. In this project we are investigating whether high glucose alters the expression of endothelial specific connexins (Cx37, Cx40, Cx43), and connexin phosphorylation.

A third project attempts to unravel the mechanism(s) underlying blood retinal barrier breakdown in diabetic retinopathy. Because tight junction serves as the permeability barrier we are currently investigating whether the synthesis of occludin and ZO-1, and other endotheli  al tight junction proteins are altered by high glucose condition in vitro and in retinal capillaries of diabetic rats.

A fourth project attempts to identify a biochemical link between the pathogenesis of diabetic retinopathy and glaucoma from the perspective of high glucose-induced overexpression of ECM proteins in trabecular meshwork and Schlemm’s canal. Related to this project, we are also investigating if high HbA1c levels are linked to increased IOP in glaucomatous patients.

Recent publications:

Roy S, Zhang K, Roth T, Vinogradov S, Kabanov A. Reduction of fibronectin expression by intravitreal administration of antisense oligonucleotides in rat retina. Nature Biotechnol. 17(5):476-9, 1999.

Roy S, Sato T, Paryani G, and Kao R. Downregulation of Fibronectin Overexpression Reduces Basement Membrane Thickening and Vascular Lesions in Retinas of Galactose-fed Rats. Diabetes, 52(5):1229-34, 2003.

Oshitari T, Polewski P, Chadda M, Li AF, Sato T, Roy S. Effect of combined AS-oligos against high glucose- and diabetes-induced overexpression of extracellular matrix components and increased vascular permeability. Diabetes 55:86-92, 2006.

Oshitari T and Roy S. Common therapeutic strategies for diabetic retinopathy and glaucoma. Current Drug Therapy 2(3): 224-232, 2007.

Behl Y, Krothapalli P, Desta T, DiPiazza A, Roy S, Graves DT. Diabetes-enhanced TNF-a Production Promotes Apoptosis and the Loss of Retinal Microvascular Cells in Type 1 and Type 2 Models of Diabetic Retinopathy. Am J of Pathol, 172: 1411-1418, 2008.

Oshitari T, Yamamoto S, Hata N, Roy S. Mitochondria- and caspase-dependent cell death pathway involved in neuronal degeneration in diabetic retinopathy. British Journal of Ophthalmology, 92:552-556, 2008.

Cherian S, Roy S, Pinheiro A, Roy S. Tight glycemic control reduces fibronectin overexpression and basement membrane thickening in retinal and glomerular capillaries of diabetic rats. Invest Ophthalmol Vis Sci, 50:943-949, 2009.

Behl Y, Krothapalli P, Desta T, Roy S, Graves DT. FOXO1 Plays an Important Role in Enhanced Microvascular Cell Apoptosis and Microvascular Cell Loss in Type 1 and Type 2 Diabetic Rats. Diabetes 58(4):917-25, 2009.

Technologies available for sharing upon request:

Retinal vascular network isolation