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Douglas M. BurnsResearch Associate Professor
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Vanderbilt University, Ph.D., 1982; Postdoctoral Research Fellow, Case Western-Reserve University; Research Associate, University of Washington-Seattle and the Calcium Metabolism Laboratory, American Lake Veterans Affairs Medical Center; Research Assistant Professor, University of Miami and the Miami Veterans Affairs Medical Center; Director of the Bone Cell Biochemistry Laboratory, Kansas City Veterans Affairs Medical Center; Research Assistant Professor, University of Kansas Medical Center.
The current focus of my work is on the interaction between bioactive peptides and steroids in the regulation of bone cell maturation and phenotypic function. Bioactive peptides of immediate interest include known skeletal neuroeffectors (i.e., CGRP, VIP, and NPY), known hormones (i.e., parathyroid hormone, calcitonin), and other endogenous factors (i.e., G/M-CSF, bone morphogenetic proteins, epidermal growth factor, IGF-I). Steroids under investigation include 1,25-dihydroxyvitamin D3, glucocorticoids, and adrenal androgen (DHEA and DHEA-S). One long-term goal is to develop an understanding of the molecular and cellular mechanisms activated by the actions/interactions of these biological factors in their regulation of osteoblasts and osteoclasts with a view towards developing novel therapies for metabolic bone diseases such as osteoporosis.
In addition, my laboratory is currently developing in vitro model systems that will facilitate examination of the cellular and molecular mechanisms that drive scleorotic and lytic processes in bone metastatic prostate cancer.
Kawase, T., Orikasa, M. and Burns, D.M. (1998) 1,25-Dihydroxyvitamin D3 modulates the actions of phorbol 12-myritate 13-acetate or dimethylsulfoxide to induce differentiation of human promyelocytic cells. Calcif. Tiss. Intl., in press.
Kawase, T. and Burns, D.M. (1998) Calcitonin gene-related peptide stimulates potassium efflux via ATP-sensitive potassium channels and produces membrane hyperpolarization in osteoblastic UMR106 cells. Endocrinology, in press.
Kawase, T., Orikasa, M. and Burns, D.M. (1998) Possible regulation of epidermal grown factor receptor autophosphorylation by calcium and G-proteins in chemically permeabilized rat UMR106 osteoblastic cells, minor revisions requested by editor, Archives of Oral Biology.
Kawase, T., Oguro, A. and Burns, D.M. (1996) Characteristics of NaF-induced differentiation of HL-60 cells. J. Bone Min. Res., 11: 1676-1687.
Kawase, T., Howard, G.A., Roos, B.A. and Burns, D.M. (1996) Calcitonin gene-related peptide inhibits net transmembrane Ca2+ uptake in osteoblastic cells through cAMP-independent activation of ATP-sensitive membrane K+ channels. Endocrinology, 137:984-990.
Kawase, T., Howard, G.A., Roos, B.A. and Burns, D.M. (1995) Diverse actions of calcitonin gene-related peptide (CGRP) on intracellular free Ca2+ concentration in UMR-106 osteoblast-like cells. Bone, 16:379S-384S.
Kawase, T., Orikasa, M., Ogata, S. and Burns, D.M. (1995) Protein tyrosine phosphorylation induced by epidermal growth factor and insulin-like growth factor-I in the rat clonal RDP-4.1 dental pulp-cell line. Arch. Oral. Biol., 40(10):921-930.
Kawase, T., Ogata, S., Orikasa, M. and Burns, D.M. (1995) 1,25-Dihydroxyvitamin D3 promotes prostaglandin E1-induced differentiation of HL-60 human premyelocytic cells. Calcif. Tis. Intl, 57(5):359-366.
Burns, D.M., Birnbaum, R.S. and Roos, B.A. (1989) A neuroendocrine peptide derived from the amino-terminal half of rat procalcitonin. Molecular Endocrinology 3:140-147.
Burns, D.M., Forstrom, J.E., Friday, K.E., Howard, G.A. and Roos, B.A. (1989) Procalcitonin's amino-terminal cleavage peptide (N-procalcitonin) is a bone-cell mitogen. Proceedings of the National Academy of Science (USA), 86:9519-9523.
