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Contact Information:
University of Rochester
School of Medicine and Dentistry
601 Elmwood Ave, Box 711
Rochester, New York 14642
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Medical Center, Room 4-8543
Phone: (585) 273-1770
Fax: (585) 273-2652 |
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Research Overview
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| The interaction of cells with their extracellular matrix generates a complex series
of signaling events which serve to regulate several aspects of cell behavior, including growth,
differentiation, adhesion, and motility. Fibronectins are a family of large molecular mass glycoproteins
which circulate in the plasma at high concentrations and which can be found in an insoluble form in
extracellular matrices throughout the body. At various times during development, fibronectin deposition into
the extracellular matrix is upregulated to support the functions of cell adhesion, migration and
differentiation. In addition, fibronectin expression and deposition are markedly increased in
tissues following injury, where it functions as a chemoattractant and adhesive molecule for migrating
cells. The deposition of fibronectin into the extracellular matrix is a dynamic, multistep process that
is normally tightly regulated in order to ensure controlled matrix deposition. In certain disease states,
including atherosclerosis and pulmonary fibrosis, loss of this regulation gives rise to either excess or
inappropriate fibronectin deposition.
Research in this laboratory is aimed at defining the molecular basis and cellular consequences of
increased fibronectin deposition into the extracellular matrix. In particular, we are interested in identifying
mechanisms which control and modulate fibronectin deposition in order to define strategies to limit the excess
matrix deposition of both fibronectin and collagen during pulmonary fibrosis. This project involves the use of
various biochemical, molecular, cellular and physiological techniques to determine the relationship between extracellular
matrix fibronectin and collagen synthesis and accumulation both in vitro and in the development of pulmonary fibrosis,
in vivo. Additional studies are directed at differentiating the effect of soluble, plasma fibronectin from the
effect of insoluble, extracellular matrix fibronectin in the regulation of cell migration. Fibronectin has
been shown to accumulate in parallel with the development of several forms of fibrosis, including fibrosis of the
lung. The effect of excess fibronectin deposition into the extracellular matrix on cell behavior is not
known. Understanding the influence of extracellular matrix fibronectin on cell function is essential to elucidating
the response of cells to a fibrotic matrix, where differences in the extent and composition of the extracellular matrix
may significantly alter cellular phenotypes and contribute to the progression of the disease.
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Recent Publications
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Hocking, D.C., and Chang, C.H. (2003) Fibronectin matrix polymerization regulates small airway epithelial cell migration. Am. J. Physiol. 285:L169-L179.
Gildner, C.D., Lerner, A.L., and Hocking, D.C. (2004) Fibronectin matrix polymerization increases tensile strength of model tissue. Am. J. Physiol. 287:H46-H53.
Wojciechowski, K., Chang, C.H., and Hocking, D.C. (2004) Expression, production, and characterization of full-length vitronectin in Escherichia coli. Protein Expr. Purif. 36:131-138.
PubMed Publication List
PubMed is maintained by the National
Library of Medicine
and provides complete abstracts of all 'hocking dc' publications,
as well as links to the full text of many articles (at journal
homepages).
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