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Doug Coffin
Professor

Phone: (406) 243-4723

Email: douglas.coffin@umontana.edu

Doug Coffin, Ph.D., was recently hired as an Associate Professor for Molecular Genetics in the Department of Biomedical and Pharmaceutical Sciences, School of Pharmacy and Allied Health Sciences. Doug comes to Missoula from the McLaughlin Research Institute in Great Falls where he was a Research Scientist for the last five years. He is a graduate of SUNY College at Buffalo (B.A., M.A., 1985) and the SUNY HSC at Syracuse (Ph.D., 1989). After receiving his Ph.D., Doug worked as a post-doctoral fellow at the University of Washington and the University of Cincinnati before coming to Montana.

RESEARCH STATEMENT
Most major pathologies include a problem with angiogenesis as a component or secondary complication. Angiogenesis, a.k.a. "neovascularization" for new growth of blood vessels is involved in cancer, heart disease, diabetes, and birth defects. There are a variety of molecules that regulate angiogenesis including growth factors, hormones, and metabolites. In most cases, research attempts to fundamentally understand these regulatory processes with the ultimate goal of either inhibiting or facilitating angiogenesis, depending on the pathology. For example, in cancer the goal is to inhibit angiogenesis, depriving a malignant tumor the means to obtain nutrients and dispose of nitrogenous wastes. In heart disease the goal is to facilitate angiogenesis, enhancing growth of collateral coronary arteries as the established vessels close from atherosclerosis.

The Coffin lab focuses on the structure and function of angiogenic growth factor genes, particularly the FGFs, in cardiovascular disease and other pathologies. Their approach uses transgenesis and gene targeting to create murine models and test gene function. They have succeeded in making transgenic and knockout mice for FGF-2, and mice with modifications in other cell cycle/cell proliferation genes that model tumor angiogenesis, coronary angiogenesis and human dwarfisms. Overall they have over 500 mice and more than 10 different lines of transgenic or knockout mice for their experiments.
KEY PUBLICATIONS

Bunderson, M., Pereira, F., Schneider, M.C., Shaw, P.K., Coffin, J.D. and Beall, H.D. (2006). Manganese enhances peroxynitrite and leukotriene E4 formation in bovine aortic endothelial cells exposed to arsenic. Cardiovasc Toxicol 6:15-23.

Grass, T.M., Lurie, D.I. and Coffin, J.D. (2006). Transitional angiogenesis and vascular remodeling during coronary angiogenesis in response to myocardial infarction. Acta Histochem 108:293-302.

Hurley, M.M., Okada, Y., Xiao, L., Tanaka, Y., Ito, M., Okimoto, N., Nakamura, T., Rosen, C.J., Doetschman, T. and Coffin, J.D. (2006). Impaired bone anabolic response to parathyroid hormone in Fgf2-/- and Fgf2+/- mice. Biochem Biophys Res Commun 341:989-994.

Marie, P.J., Coffin, J.D. and Hurley, M.M. (2005). FGF and FGFR signaling in chondrodysplasias and craniosynostosis. J Cell Biochem 96:888-896.

Sobue, T., Naganawa, T., Xiao, L., Okada, Y., Tanaka, Y., Ito, M., Okimoto, N., Nakamura, T., Coffin, J.D. and Hurley, M.M. (2005). Over-expression of fibroblast growth factor-2 causes defective bone mineralization and osteopenia in transgenic mice. J Cell Biochem 95:83-94.

Bunderson, M., Brooks, D.M., Walker, D.L., Rosenfeld, M.E., Coffin, J.D. and Beall, H.D. (2004). Arsenic exposure exacerbates atherosclerotic plaque formation and increases nitrotyrosine and leukotriene biosynthesis. Toxicol Appl Pharmacol 201:32-39.

Xiao, L., Naganawa, T., Obugunde, E., Gronowicz, G., Ornitz, D.M., Coffin, J.D. and Hurley, M.M. (2004). Stat1 controls postnatal bone formation by regulating fibroblast growth factor signaling in osteoblasts. J Biol Chem 279:27743-27752.

Ismail, J.A., Poppa, V., Kemper, L.E., Scatena, M., Giachelli, C.M., Coffin, J.D. and Murry, C.E. (2003). Immunohistologic labeling of murine endothelium. Cardiovasc Pathol 12:82-90.

Okada, Y., Montero, A., Zhang, X., Sobue, T., Lorenzo, J., Doetschman, T., Coffin, J.D. and Hurley, M.M. (2003). Impaired osteoclast formation in bone marrow cultures of Fgf2 null mice in response to parathyroid hormone. J Biol Chem 278:21258-21266.

Xiao, L., Liu, P., Sobue, T., Lichtler, A., Coffin, J.D. and Hurley, M.M. (2003). Effect of overexpressing fibroblast growth factor 2 protein isoforms in osteoblastic ROS 17/2.8 cells. J Cell Biochem 89:1291-1301.

Bunderson, M., Coffin, J.D. and Beall, H.D. (2002). Arsenic induces peroxynitrite generation and cyclooxygenase-2 protein expression in aortic endothelial cells: possible role in atherosclerosis. Toxicol Appl Pharmacol 184:11-18.

Sahni, M., Raz, R., Coffin, J.D., Levy, D. and Basilico, C. (2001). STAT1 mediates the increased apoptosis and reduced chondrocyte proliferation in mice overexpressing FGF2. Development 128:2119-2129.

Wishcamper, C.A., Coffin, J.D. and Lurie, D.I. (2001). Lack of the protein tyrosine phosphatase SHP-1 results in decreased numbers of glia within the motheaten (me/me) mouse brain. J Comp Neurol 441:118-133.

Brewster, J.L., Martin, S.L., Toms, J., Goss, D., Wang, K., Zachrone, K., Davis, A., Carlson, G., Hood, L. and Coffin, J.D. (2000). Deletion of Dad1 in mice induces an apoptosis-associated embryonic death. Genesis 26:271-278.

Chiotti, K., Choo, S.J., Martin, S.L., Reichert, C., Grass, T.M., Duran, C.M. and Coffin, J.D. (2000). Activation of myocardial angiogenesis and upregulation of fibroblast growth factor-2 in transmyocardial-revascularization-treated mice. Coron Artery Dis 11:537-544.

Montero, A., Okada, Y., Tomita, M., Ito, M., Tsurukami, H., Nakamura, T., Doetschman, T., Coffin, J.D. and Hurley, M.M. (2000). Disruption of the fibroblast growth factor-2 gene results in decreased bone mass and bone formation. J Clin Invest 105:1085-1093.

Fulgham, D.L., Widhalm, S.R., Martin, S. and Coffin, J.D. (1999). FGF-2 dependent angiogenesis is a latent phenotype in basic fibroblast growth factor transgenic mice. Endothelium 6:185-195.

Kuzis, K., Coffin, J.D. and Eckenstein, F.P. (1999). Time course and age dependence of motor neuron death following facial nerve crush injury: role of fibroblast growth factor. Exp Neurol 157:77-87.

Vaccarino, F.M., Schwartz, M.L., Raballo, R., Nilsen, J., Rhee, J., Zhou, M., Doetschman, T., Coffin, J.D., Wyland, J.J. and Hung, Y.T. (1999). Changes in cerebral cortex size are governed by fibroblast growth factor during embryogenesis. Nat Neurosci 2:848.

Naski, M.C., Colvin, J.S., Coffin, J.D. and Ornitz, D.M. (1998). Repression of hedgehog signaling and BMP4 expression in growth plate cartilage by fibroblast growth factor receptor 3. Development 125:4977-4988.

Zhou, M., Sutliff, R.L., Paul, R.J., Lorenz, J.N., Hoying, J.B., Haudenschild, C.C., Yin, M., Coffin, J.D., Kong, L., Kranias, E.G., Luo, W., Boivin, G.P., Duffy, J.J., Pawlowski, S.A. and Doetschman, T. (1998). Fibroblast growth factor 2 control of vascular tone. Nat Med 4:201-207.