Dr. Medici's research focuses on cell plasticity and its role in mediating the progression of human diseases. In particular, his lab studies how epithelial-mesenchymal transition (EMT) and endothelial-mesenchymal transition (EndMT) contribute to pathological processes such as cancer metastasis, organ fibrosis, and heterotopic ossification. The Medici lab also studies tumor angiogenesis and the mechanisms that give rise to the formation of vascular tumors. Dr. Medici's breakthrough discovery of endothelial-derived stem cells has laid the foundation for a novel approach of using blood vessels to regenerate tissues for the treatment of degenerative diseases, which is currently the primary focus of his lab.

Biography

Dr. Medici is an Assistant Professor of Orthopaedics and Medicine at the Warren Alpert Medical School of Brown University. He received his Ph.D. from Harvard University and did his postdoctoral training at Harvard Medical School and the Beth Israel Deaconess Medical Center. He was an Instructor of Medicine and Developmental Biology at Harvard Medical School prior to joining the faculty at Brown. Dr. Medici is the Director of the Laboratory for Regenerative Medicine and a member of the Cardiovascular Research Center at Rhode Island Hospital. His research interests include cancer biology, vascular biology, skeletal diseases, stem cells and tissue regeneration.

Selected Publications

• Susienka, M. and Medici, D. (2013). Vascular endothelium as a novel source of stem cells for bioengineering. Biomatter 3, e24647.(2013)
• Medici, D. and Olsen, B.R. (2012). Transformation of Vascular Endothelial Cells into Multipotent Stem-Like Cells: Role of the Activin-Like Kinase-2 Receptor. Stem Cells and Cancer Stem Cells: Therapeutic Applications in Disease and Injury. Springer. Volume 8, Chapter 19.(2012)
• Medici, D. and Olsen, B.R. (2012). The role of endothelial-mesenchymal transition in heterotopic ossification. J. Bone Miner. Res. 27, 1619-1622.(2012)
• Medici, D. and Olsen, B.R. (2012). Rapamycin inhibits proliferation of hemangioma endothelial cells by reducing HIF-1-dependent expression of VEGF. PLoS One 7, e42913.(2012)
• Medici, D. and Kalluri, R. (2012). Endothelial-mesenchymal transition and its contribution to the emergence of stem cell phenotype. Semin. Cancer Biol. 22, 379-384.(2012)
• Suh, N., Paul, S., Lee, H.J., Yoon, T., Shah, N., Son, A., Zhou, R., Reddi, A.H., Medici, D., and Sporn, M.B. (2012). Synthetic triterpenoids, CDDO-imidazolide and CDDO-ethyl amide, induce chondrogenesis. Osteoarthritis Cartilage 20, 446-450.(2012)
• Medici, D. and Olsen, B.R. (2011). Transforming blood vessels into bone. Cell Cycle 10, 362-363.(2011)
• Medici, D., Potenta, S., and Kalluri, R. (2011). TGF-beta2 promotes Snail-dependent endothelial-mesenchymal transition through convergence of Smad-dependent and Smad-independent signaling. Biochem. J. 437, 515-520.(2011)
• Walsh, L.A., Nawshad, A., and Medici, D. (2011). Discoidin domain receptor 2 is a critical regulator of epithelial-mesenchymal transition. Matrix Biol. 30, 243-247.(2011)
• Medici, D. and Nawshad, A. (2010). Type I collagen promotes epithelial-mesenchymal transition through ILK-dependent activation of NF-κB and LEF-1. Matrix Biol. 29, 161-165.(2010)
• Medici, D., Shore, E.M., Lounev, V., Kaplan, F.S., Kalluri, R., and Olsen, B.R. (2010). Conversion of vascular endothelial cells into multipotent stem-like cells. Nat. Med. 16, 1400-1406.(2010)
• Kizu, A., Medici, D., and Kalluri, R. (2009). Endothelial-mesenchymal transition as a novel mechanism for generating myofibroblasts during diabetic nephropathy. Am. J. Pathol. 175, 1371-1373.(2009)
• Medici, D., Razzaque, M.S., DeLuca, S., Rector, T.L., Hou, B., Kang, K., Goetz, R., Mohammadi, M., Kuro-o, M., Olsen, B.R., and Lanske, B. (2008). FGF-23−Klotho signaling stimulates proliferation and prevents vitamin D-induced apoptosis. J. Cell Biol. 182, 459-465.(2008)
• Medici, D., Hay, E.D., and Olsen, B.R. (2008). Snail and Slug promote epithelial-mesenchymal transition through beta-catenin−T-cell factor-4-dependent expression of transforming growth factor-beta3. Mol. Biol. Cell 19, 4875-4887.(2008)
• Jinnin, M., Medici, D., Park, L., Limaye, N., Liu, Y., Boscolo, E., Bischoff, J., Vikkula, M., Boye, E., and Olsen, B.R. (2008). Suppressed NFAT-dependent VEGFR1 expression and constitutive VEGFR2 signaling in infantile hemangioma. Nat. Med. 14, 1236-1246.(2008)
• Nawshad, A., Medici, D., Liu, C.C., and Hay, E.D. (2007). TGFbeta3 inhibits E-cadherin gene expression in palate medial-edge epithelial cells through a Smad2−Smad4−LEF1 transcription complex. J. Cell Sci. 120, 1646-1653.(2007)
• Medici, D., Hay, E.D., and Goodenough, D.A. (2006). Cooperation between snail and LEF-1 transcription factors is essential for TGF-beta1-induced epithelial-mesenchymal transition. Mol. Biol. Cell 17, 1871-1879.(2006)