Thomas N. Wight, PhD
Background Information
Dr. Wight completed his undergraduate degree at the University of Maine and his graduate degree (PhD) at the University of New Hampshire. His post-doctoral training was at the Department of Pathology at the University of Washington in Seattle. Following post-doctoral training, he moved back to New England and joined the faculty in Cell Biology at the University of New Hampshire as an Assistant Professor. He rejoined the Department of Pathology at the University of Washington in 1979 and was promoted to Full Professor in 1988. In 2000, he joined The Hope Heart Institute in Seattle as Chair of Vascular Biology and remained an Affiliate Professor of Pathology at the University of Washington School of Medicine. He has been named an Established Investigator of the American Heart Association, served on National Institutes of Health and American Heart Association Study Sections, and served on several editorial boards. Dr. Wight served as Co-Chair of the Proteoglycan Gordon Conference in 2008. His research focuses on the role of proteoglycans in regulating cell phenotype and extracellular matrix assembly. He has published over 290 articles on proteoglycans and hyaluronan. He is currently Director of the Matrix Biology Program at the Benaroya Research Institute at Virginia Mason.
Area of Research
Projects in Dr. Wight’s Laboratory involve defining the role that proteoglycans play in vascular diseases including atherosclerosis and restenosis, diseases of the lung such as asthma and autoimmune diseases such as type 1 diabetes. Special emphasis is placed on how these extracellular matrix molecules influence events associated with inflammation. Other projects involve developing the use of proteoglycan genes and products of those genes to bioengineer vascular tissue in order to maintain normal vasculature structure. Specific projects in this area include evaluating the mechanism(s) by which proteoglycans influence extracellular matrix assembly such as formation of elastic fibers. Projects related to this tissue engineering approach include developing “designer extracellular matrices” to be used in the treatment and engineering of tissues destroyed by trauma and/or disease.
Featured Publications
Potter-Perigo S, Johnson PY, Evanko SP, Chan CK, Braun KR, Wilkinson TS, Altman LC, Wight TN. Polyinosine-polycytidylic acid stimulates versican accumulation in the extracellular matrix promoting monocyte adhesion. Am J Resp Cell Molec Biol. 43:109-20, 2010. PMCID: PMC2911565
Chan CK, Rolle MW, Potter-Perigo S, Braun KR, Van Biber BP, Laflamme MA, Murry CE, Wight TN. Differentiation of cardiomyocytes from human embryonic stem cells is accompanied by changes in the extracellular matrix production of versican and hyaluronan. J Cell Biochem. 111:585-96, 2010. PMCID: PMC2946489
Merrilees MJ, Beaumont BW, Braun KR, Thomas AC, Kang I, Hinek A, Passi A, Wight TN. Neointima formed by arterial smooth muscle cells expressing versican variant V3 is resistant to lipid and macrophage accumulation. Arterioscler Thromb Vasc Biol. 31:1309-1316, 2011. PMCID: PMC3123728
Evanko SP, Potter-Perigo S, Bollyky PL, Nepom GT, Wight TN. Hyaluronan and versican in the control of human T lymphocyte adhesion and migration. Matrix Biol. 31:90-100, 2012. PMCID: PMC3288568
Chang MY, Chan CK, Braun KR, Green PS, O’Brien KD, Chait A, Day AJ, Wight TN. Monocyte-to-macrophage differentiation: Synthesis and secretion of a complex extracellular matrix. J Biol Chem. 287:14122-14135, 2012. PMCID: PMC3340194
Bollyky PL, Bogdani M, Bollyky J, Hull R, Wight TN. The role of hyaluronan and the extracellular matrix in islet inflammation and immune regulation. Curr Diab Rep. 12:471-80, 2012. PMCID: PMC3432646 [Available on 2013/10/1]
Hull RL, Johnson PY, Braun KR, Day AJ, Wight TN. Hyaluronan and hyaluronan binding proteins are normal components of mouse pancreatic islets and are differentially expressed by islet endocrine cell types. J Histochem Cytochem. 60:749-60, 2012. PMCID: PMC3524560
Obika M, Vernon RB, Gooden MD, Braun KR, Chan CK, Wight TN. ADAMTS-4 and biglycan are expressed at high levels and co-localize to podosomes during endothelial cell tubulogenesis in vitro. J Histochem Cytochem. 62:34-49, 2014. PMCID: PMC3873805
Wight TN, Kang I, Merrilees MJ. Versican and the control of inflammation. Matrix Biol. 35:152-61, 2014. PMCID: PMC4039577
Bogdani M, Johnson PY, Potter-Perigo S, Nagy N, Day AJ, Bollyky PL, Wight TN. Hyaluronan and hyaluronan binding proteins accumulate in both human type 1 diabetic islets and lymphoid tissues and associate with inflammatory cells in insulitis. Diabetes. 63:2727-2743, 2014. PMCID: PMC4113060
Reeves SR, Kolstad T, Lien T-Y, Elliott M, Ziegler SF, Wight TN, Debley JS. Asthmatic airway epithelial cells differentially regulate fibroblast expression of extracellular matrix components. J Allergy Clin Immunol. 134:663-670, 2014. PMCID: PMC4149938
Kang I, Yoon DW, Braun KR, Wight TN. Expression of versican V3 by arterial smooth muscle cells alters TGFβ-, EGF-, and NFkB-dependent signaling pathways, creating a microenvironment that resists monocyte adhesion. J Biol Chem. 289:15393-15404, 2014. PMCID: PMC4140896
Keire PA, Bressler SL, Lemire JM, Edris B, Rubin BP, Rahmani M, McManus BM, van de Rijn M, Wight TN. A role for versican in the development of leiomyosarcoma. J Biol Chem. 289:34089-103, 2014. PMCID: PMC4256343
Evanko SP, Potter-Perigo S, Petty LJ, Workman GA, Wight TN. Hyaluronan controls the deposition of fibronectin and collagen and modulates TGF-β1 induction of lung myofibroblasts. Matrix Biol. 42:74-92, 2015. PMCID: PMC4524654
Hull RL, Bogdani M, Nagy N, Johnson PY, Wight TN. Hyaluronan: A mediator of islet dysfunction and destruction in diabetes? J Histochem Cytochem. 8:592-603, 2015. PMCID: PMC4530396
Kang I, Barth JL, Sproul EP, Yoon DW, Workman GA, Braun KR, Argraves WS, Wight TN. Expression of V3 versican by rat arterial smooth muscle cells promotes differentiated and anti-inflammatory phenotypes. J Biol Chem. 290:21629-41, 2015. PMCID: PMC4571886
