BBS Faculty Member - Bjorn Olsen

Bjorn Olsen

Department of Developmental Biology

Harvard School of Dental Medicine
Developmental Biology REB 409B
188 Longwood Ave
Boston, MA 02115
Tel: 617-432-1874
Fax: 617-432-0638
Email: bjorn_olsen@hms.harvard.edu
Lab Members: 10 postdoctoral fellows, 1 graduate student



Research Activities

My laboratory studies skeletal and vascular morphogenesis, growth and remodeling/repair. Work is currently directed at three project areas.

In the first project we study pathogenetic mechanisms of infantile hemangioma, the most common tumor in childhood. Occurring in up to 10% of Caucasian infants, hemangiomas go through a period of high proliferative activity during the first year of life before they involute and undergo regression to a fibro-fatty residue. We have identified signaling abnormalities in hemangioma endothelial cells that provide an explanation for the rapid growth of the tumors and are currently studying the mechanisms responsible for the slow involution and regression. Our goal is to develop strategies for controlling the proliferation of the tumors, and inducing their involution at an early stage.

In the second project we investigate mechanisms that control the development and homeostasis of cartilage and bone, using a combination of human and mouse genetics and studies of cells in culture. In recent studies we have also identified processes by which vascular endothelial cells transition to mesenchymal stem-like cells and differentiate to cartilage and bone in patients with a genetic disorder of progressive ectopic bone formation.

In the third project we have been studying genetic causes of degenerative joint disease (osteoarthritis) in humans and mice. One approach involves identification of mutations responsible for early-onset osteoarthritis as part of inherited osteochondrodysplasias and cellular/molecular analyses of pathogenetic mechanisms.



Last Update: 8/22/2013



Publications

For a complete listing of publications click here.

 


 

Ueki, Y, Lin, C-Y, Senoo, M, Ebihara, T, Agata, N, Onji, M, Saheki, Y, Kawai, T, Mukherjee, PM, Reichenberger, E, Olsen, BR. Increased myeloid cell responses to M-CSF and RANKL cause bone loss and inflammation in Sh3bp2 “cherubism” mice. Cell, 2007, 128:71-83.

Saharinen, P, Eklund, L, Miettinen, J, Wirkkala, R, Anisimov, A, Winderlich, M, Nottebaum, A, Vestweber, D, Deutsch, U, Koh, GY, Olsen, BR, Alitalo, K. Angiopoietins assemble distinct Tie2 signalling complexes in endothelial cell-cell and cell-matrix contacts. Nat Cell Biol., 2008 10:527-537.

Jinnin, M, Medici, D, Park, L, Limaye, N, Liu, Y, Boscolo, E, Bischoff, J, Viikkula, M, Boye, E, Olsen, BR. Suppressed NFAT-dependent VEGFR1 expression and constitutive VEGFR2 signaling in infantile hemangioma. Nat. Med., 2008, 14:1236-1246.

Medici, D, Shore, EM, Lounev, VY, Kaplan, FS, Kalluri, R, Olsen, BR. Conversion of vascular endothelial cells into multipotent stem-like cells. Nat Med 2010, 16: 1400-1406.

Liu, Y, Jia, S, Lotinun, S, Baron, R, Ferrara, N, Olsen, BR. VEGF stimulates trabecular bone formation and suppresses marrow adipogenesis in mice by intracrine mechanisms. JCI, 2012, September, on line.



© 2013 by the President and Fellows of Harvard College