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Damian Medici Assistant Professor of Orthopaedics, Assistant Professor of Medicine

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 also the Director of the Center for Regenerative Medicine and a member of the Cardiovascular Research Center. His research interests include cancer biology, vascular biology, skeletal diseases, stem cells and tissue regeneration.

Brown Affiliations

scholarly work

LIang, O.D., Reginato, A.M., and Medici, D. (2015). Apyrase as a novel therapeutic inhibitor of heterotopic ossification. Annals of Translational Medicine 3, S32.

Yang, N., Reginato, A.M., and Medici, D. (2015). Basic Science and Pathogenesis of Heterotopic Ossification. Heterotopic Ossification: Basic Science, General Principles, and Clinical Correlates in Orthopaedic Surgery. Nova Science Publishing. Chapter 1.

Gonzalez, D.M. and Medici, D. (2014). Signaling mechanisms of the epithelial-mesenchymal transition. Science Signaling 7, re8.

Ramirez, D.M., Ramirez, M.R., Reginato, A.M., and Medici, D. (2014). Molecular and cellular mechanisms of heterotopic ossification. Histology and Histopathology 29, 1281-1285. 

Susienka, M.J. and Medici, D. (2013). Vascular endothelium as a novel source of stem cells for bioengineering. Biomatter 3, e24647.

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 and Cartilage 20, 446-450.

Medici, D. and Kalluri, R. (2012). Endothelial-mesenchymal transition and its contribution to the emergence of stem cell phenotype. Seminars in Cancer Biology 22, 379-384.

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.

Medici, D. and Olsen, B.R. (2012). The role of endothelial-mesenchymal transition in heterotopic ossification. Journal of Bone and Mineral Research 27, 1619-1622.

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.

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. Biochemical Journal 437, 515-520.

Walsh, L.A., Nawshad, A., and Medici, D. (2011). Discoidin domain receptor 2 is a critical regulator of epithelial-mesenchymal transition. Matrix Biology 30, 243-247.

Medici, D. and Olsen, B.R. (2011). Transforming blood vessels into bone. Cell Cycle 10, 362-363.

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. Nature Medicine 16, 1400-1406.

Medici, D. and Nawshad, A. (2010). Type I collagen promotes epithelial-mesenchymal transition through ILK-dependent activation of NF-κB and LEF-1. Matrix Biology 29, 161-165.

Kizu, A., Medici, D., and Kalluri, R. (2009). Endothelial-mesenchymal transition as a novel mechanism for generating myofibroblasts during diabetic nephropathy. American Journal of Pathology 175, 1371-1373.

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. Nature Medicine 14, 1236-1246.

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. Molocular Biology of the Cell 19, 4875-4887.

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. Journal of Cell Biology 182, 459-465.

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. Journal of Cell Science 120, 1646-1653.

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. Molecular Biology of the Cell 17, 1871-1879.

research overview

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 cause the formation of vascular tumors. Dr. Medici's groundbreaking 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.

funded research

Endothelial Plasticity in Human Disease (R01HL112860)
National Heart, Lung and Blood Institute
National Institutes of Health

Mechanisms of Heterotopic Ossification (P20GM104937)
National Institute of General Medical Sciences
National Institutes of Health

Molecular and Cellular Mechanisms of Hemangioma Progression
The John Butler Mulliken Foundation