Faculty Member

Scientific Interests

Edward Puzas Ph.D.

Looking to harness the biology of the skeletal system to create a new class of treatment for osteoporosis, arthritis and cancer. Experiments underway explore how bone cells (osteoclasts and osteoblasts) remove and replace aging and damaged bone, and the chemical signals that drive the process. Under examination are proteins like transforming growth factor beta, epidermal growth factor and basic fibroblast growth factor, each of which may be manipulated to reverse bone loss.

Di Chen, M.D., Ph.D.

Bone morphogenetic proteins (BMPs) and Wnt proteins are families of signaling enzymes central to bone disorders, especially in congenital defects that develop in the human embryo. Chen's team is focused on the role of BMP and Wnt signaling mechanisms in osteoclasts, which dissolve aging bone, and osteoblasts, which fill in the craters left by osteoclasts with new bone. Chemical signaling between the two cell types must be perfect, or bone is not replaced as quickly as it is dissolved (osteoporosis).

Hicham Drissi, Ph.D.

Among the proteins that regulate blood cell construction in bone marrow and the storage of minerals (e.g. calcium) in bone are the Runt homology transcription factors. Evidence is mounting that Runt factors contribute to diseases including acute myeloid leukemia and gastric cancer. Drissi's lab is using cellular and molecular biology tools to establish the role of these factors in skeletal and cartilage development, as well as in stem cell differentiation.

Edward Schwarz, Ph.D.

Interested in nuclear factor kappa B (NFκB), a regulatory protein that starts the process by which stored DNA directions are "read and followed" to create proteins with specific jobs in the right cells at certain times. NFκB switches on genes involved in the immune system's response to stress (e.g. bacteria, viruses, ultraviolet light), including those that code for the creation of interleukins and tumor necrosis factor alpha. Genetic mistakes involving the NFκB pathway have been observed in autoimmune disease (e.g. rheumatoid arthritis) and in cancers like lymphoma. Agents that block NFκB activity would have tremendous therapeutic value, and Schwartz' lab is working to design such drug and gene therapies.

Michael Zuscik, Ph.D.

In the womb, the human skeleton is made of cartilage, but most of it matures to become bone as we age. Zuscik's lab is focused on the cellular and molecular processes that govern cartilage development in the womb, as part of disease and during healing. Specifically, Zuscik's lab are interested in the process by which stem cells - embryonic and unspecialized - "decide" to mature into either bone or cartilage. Determining those mechanisms would advance the treatment of arthritis and bone trauma. One project is looking into how nicotine, known to impair skeletal healing, may reduce the otherwise strong "commitment" of stem cells to become mature bone.

Randy N. Rosier, M.D., Ph.D.

Rosier's team has uncovered a critical gene that codes for an enzyme that drives the process of osteoarthritis, the gradual loss of the cartilage in joints. The team hopes to develop a method for reversing the gene's action. Other work includes the development of an arthroscopic technique that uses lasers to repair cartilage using light-activated gene therapy. Lastly, Rosier oversees an NIH-supported project using a state-of-the-art measurement device to determine whether exposure to lead may cause genetic changes in bone that lead to osteoporosis.

Xinping Zhang, Ph.D.

Focused on the exact mechanisms by which the skeleton repairs and regenerates bone. Zhang's team is devising tissue engineering and gene therapy approaches to enhance bone repair. The first step: clarify the chemical signals controlling whether cells in an embryo's mesoderm go on to form either connective tissue, bone, cartilage or circulatory and lymphatic cells. Similar processes regulate bone healing later in life.

Hani Awad, Ph.D.

Tissue engineering uses living cells as engineering materials to improve or replace human tissue. Replacement parts include cartilage repaired with living chondrocytes, or cartilage cells. Awad's lab is working to understand the role of physical factors (fluid flow, oxygen levels) and chemical factors (growth factors, cytokines, and hormones) play in regulating the growth and metabolism of stem cells in tissue-engineered cartilage and bone.