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Cell-cell and cell-extracellular matrix (ECM) adhesion
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Dr. Stanley Hoffman is a Professor in the Division of Rheumatology & Immunology and in the Department of Cell Biology at the Medical University of South Carolina. He received a B.Sc. in Life Sciences from the Massachusetts Institute of Technology in 1972 and a Ph.D. in Cell Biology from the California Institute of Technology in 1978. He then worked with Nobel Laureate Gerald M. Edelman at the Rockefeller University as a Postdoctoral Fellow, Research Associate, and Assistant Professor. He joined the Division of Rheumatology and Immunology as an Associate Professor in 1990 and was promoted to Professor in 1998.
Dr. Hoffman has been involved in the study of cell-cell and cell-extracellular matrix (ECM) adhesion since the study of the role of specific molecules in these processes was initiated in the 1970s. He has done pioneering work on several of these molecules including NCAM, tenascin-C, chondroitin sulfate proteoglycans, and periostin. The function of the ECM is critical in regulating diverse cellular processes including cell division, cell migration, differentiation, and cell death. These are the primary processes of tissue morphogenesis. When properly coordinated these processes lead to favorable outcomes such as embryonic development and the repair of damaged tissues in adult organisms. On the other hand, these processes are not properly coordinated in birth defects and in fibrotic diseases (e.g. scleroderma) in which overexpression of ECM proteins occurs.
Dr. Hoffman’s current interests focus on the identification of cells that overexpress ECM proteins in fibrotic diseases and the molecular mechanisms that regulate ECM protein overexpression. The classical viewpoint was that the cells that overexpress ECM proteins were resident cells in the affected tissue. However, recent studies suggest that a major portion of these cells are bone marrow-derived cells that differentiate into collagen-producing cells while migrating into affected tissues. A variety of studies from our lab suggest that the differentiation of bone marrow-derived cells into collagen-producing cells, their production of collagen, and their migration into tissues are all promoted by decreased expression of the master signaling molecule caveolin-1. Therefore, caveolin-1 is an outstanding target for novel treatments for fibrotic diseases which is of the utmost importance to patients because there are currently no FDA-approved treatments for these devastating diseases. Work in this area has led Dr. Hoffman and his close colleague Dr. Tourkina to patent a drug that targets caveolin-1 deficiency and to form a faculty spin-off company to participate in the development of this drug.
Work in the Hoffman laboratory has been supported by grants from the Scleroderma Foundation; NIH Heart, Lung, and Blood Institute; NIH National Center for Research Resources; NIH Institute of Aging; NIH National Center for Complementary and Alternative Medicine; American Heart Association; Department of Defense; Department of Energy; NASA; RGK Foundation; and Showa Denko K K Pharmaceutical.
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