|
Bjorn R. Olsen, MD, PhD
Hersey Professor of Cell Biolog
Dean for Research
Department of Developmental Biology
Office: REB 409
Telephone: 617-432-1874
Email: bjorn_olsen@hms.harvard.edu
Associate Professor: |
Donald Glotzer, MD |
| Instructor: |
Eileen Boye, PhD, Anthony Reginato, MD, PhD,
Chin-Yu Lin, DMD, Yasuyoshi Ueki, MD, PhD
|
Postdoctoral Research
Associate: |
Naomi Fukai, MD, PhD, Elona Kolpakova, PhD,
Alexander Marneros, MD, Masatoshi Jinnin, MD, PhD,
Christian Pfeffer, MD, Sylvia Sardi, PhD
Claudia Marilena Nicolae, PhD
|
| Research Assistant: |
Sofiya Plotkina, MS |
| PhD Student: |
Wei Huang, Damian Medici, Yanqiu Liu,
|
| Administrative Assistant: |
Yulia Pittel, MS 617-432-2359 |
Click
here for a list of Dr. Olsen's available
publications in PubMed
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 skeletal morphogenesis and growth. We are interested
in genes that control differentiation of mesenchymal cells to chondrocytes
and osteoblasts, the control of spatial patterns of mesenchymal condensations
during skeletal development and tooth formation, the molecular mechanisms
controlling the formation of ossification centers, the regulation of proliferation
and differentiation of chondrocytes in growth plates, and molecular mechanisms
responsible for accrual of bone mass and remodeling of the vertebrate skeleton.
In addition to using knock-out, knock-in, and conditional knock-out mice in
studies of specific genes, we make extensive use of genetic approaches in
mice and humans. This includes mapping of inherited disorders, gene identification
and mutation detection.
In the second project, we investigate the molecular basis for vascular morphogenesis, using a combination of human genetics of vascular tumors and malformations and studies of cells in culture. In addition, we study mice with inactivated alleles for collagens that are expressed in vascular cells, and use conditional knock-out techniques to inactivate VEGF and its receptors in mice.
In the third project, we are studying genetic causes of degenerative joint disease (osteoarthritis) in humans and mice. The approach involves identification of mutations responsible for early-onset osteoarthritis as part of inherited osteochondrodysplasias and cellular/molecular analyses of pathogenetic mechanisms.
|