Friends, colleagues, former students—even competitors—celebrated the personal and professional achievements of Harvard scientist Bjorn Olsen, intrepid explorer of the extracellular matrix, at a symposium April 14 and 15 organized by Olsen’s former mentees. In tribute to their teacher and guide, speakers traced their own successes in the field to the broad, sturdy foundation of Olsen’s pioneering research.
“Without a doubt, he’s the most brilliant man I’ve ever met,” said Damian Medici, a Dean’s Scholar at the Harvard School of Dental Medicine and an instructor of developmental biology. “He’s also the kindest and most generous man I’ve ever known.”
Scholars echoed those sentiments during the two-day event, which included a “Science Blast,” a series of 31 short research reports, followed by a day of formal lectures and posters in the Joseph B. Martin Conference Center rotunda.
Olsen, who is the Hersey Professor of Cell Biology at HMS and both professor of developmental biology and dean for research at the Harvard School of Dental Medicine, arrived at Harvard in 1985 and has published more than 360 papers. The symposium, planned by former trainees Marion (Emmy) Gordon, Donald Gerecke, Kathy Svoboda and Matthew Warman, the Harriet M. Peabody Professor of Orthopedic Surgery at Children’s Hospital Boston, who now head research programs in New Jersey, Texas and Massachusetts, was inspired by Olsen’s recent findings connecting skeletal development and vascular biology. The event probed the complex relationships between living cells and the extracellular matrix, or ECM.
Olsen has taken the lead in sorting out the ECM’s role in building and maintaining the human body from embryo to adulthood. Like mortar, the matrix binds cells together, enabling trillions to work in harmony while providing physical support and organization in higher organisms. The ECM also serves as a storehouse, transport system and source of enzymes and signaling molecules that orchestrate cellular activity.
Fundamentally, the ECM is essential to multi-cellular life: Its existence was a prerequisite for the evolution of higher organisms, and it is key to maintaining their metabolic equilibrium. Depending on the tissue or organ, the ECM contains molecules that stimulate cell growth, control cell migration or govern cell differentiation.
Numerous diseases and malformations stem from problems in the ECM and alterations in cellular interactions with the ECM. These range from tumor-like masses known as hemangiomas to deformed skeletal growth patterns and eye disorders.
Among Olsen’s major achievements are an improved understanding of dwarfism, congenital vascular anomalies, osteoporosis and osteoarthritis. His lab has also uncovered complex roles played by gene transcription factors and cell-surface receptors that, for example, rearrange blood vessel networks.
Follow the LeaderSymposium speakers noted that Olsen is good at getting people from different disciplines to talk to one another about how biological systems interact—and fail. “In the past, the muscle people and the bone people were totally uninterested in each other, but it’s remarkable how well they’ve come together,” Olsen said.
As a first-year orthodontic resident in search of a research mentor in 1986, Reginald Taylor followed a fellow resident’s tip and contacted Olsen, who “taught me how to ask the right questions,” said Taylor, now director of predoctoral orthodontics at Texas A&M Health Science Center Baylor College of Dentistry. “He has this depth of knowledge, but his knowledge doesn’t intimidate you.”
Suneel Apte, a member of the research faculty at the Cleveland Clinic, in Ohio, whose interests lie in protein regulation in the ECM, confessed that “I didn’t know anything” as a postdoctoral fellow in Olsen’s lab in 1989. At first, he said of Olsen, “I thought he was quite mad, which was very appealing.” Clearly, adventures were in store. Here was a leader worth following.
Francesco Ramirez, professor of medicine and cardiology at the Mount Sinai Medical Center, in New York, said that when in 1979 he got to Rutgers Medical School, now the Robert Wood Johnson Medical School, Olsen “took away my anxiety” while helping shape his career. Ramirez now studies connective tissue diseases. His work on Marfan syndrome led to identification of the causative gene defect.
Olsen’s team and collaborators recently reported on fibrodysplasia ossificans progressiva, a “rare but horrific disease,” Olsen said, in which endothelial cells, which line blood vessels, transform themselves into stem-like cells that give rise to bone and cartilage cells. “Patients have bone developing in soft tissues, such as muscle, causing them to lose mobility—they are frozen in space.”
The findings may open a door toward tissue repair, provided scientists can learn to control this quality of “endothelial stemness” to replace sick or dying cells. Said Olsen: “That’s what I’ll be working on in the next 10 years.”
