Chris Chen, PhD

Appointments

Assistant Scientist, Hospital for Special Surgery

Assistant Professor, New York Center for Biomedical Engineering

Visiting Assistant Professor, Department of Biomedical Engineering, City College of New York, City University of New York

 

Selected Publications

Lin P. M., Chen C. T., Torzilli P. A. (2004) Increased localization of stromelysin-1 and proteoglycan degradation in Mechanically Injured Articular Cartilage. Osteoarthritis and Cartilage. 12:485-496.

Chen C.T., Bhargava M., Lin P. M., and Torzilli P. A. (2003) Time, stress, and location dependent chondrocyte death and collagen damage in cyclically loaded articular cartilage. J. Orthopaedic Research 21:888-898.

Chen C. T., Torzilli P. A., Fishbein K. W., Spencer R. G. S., Hilger A. and Horton W.E., Jr. (2003) Matrix fixed charge density as determined by magnetic resonance microscopy of bioreactor-derived hyaline cartilage correlates with biochemical and biomechanical properties. Arthritis & Rheumatism 48(4):1047-56.

Chen C. T., Burton-Wurster N. I., Borden C., Hueffer K., Bloom S. E., and Lust G. (2001) Chondrocyte necrosis and apoptosis in impact damaged articular cartilage. J. Orthopaedic Research 19: 703-711.

Chen C. T., Burton-Wurster N. I., Lust G., Bank R. A., and Tekoppele J. M. (1999) Compositional and metabolic changes in damaged cartilage are peak-stress, stress-rate and loading-duration dependent. J. Orthopaedic Research 17: 870-879. J. Orthopaedic Research 17: 870-879.

For more publications, please see the PubMed listing.  

Research Description

Cartilage Degeneration and Regeneration

Arthritis, in the simplest terms, is the wearing away of articular cartilage. Minor damage to cartilage as a result of sports injury, trauma, or joint inflammation can often lead to progressive degeneration in cartilage matrix. It is now known that such degeneration is due mainly to the accumulation and activation of a group of enzymes called metalloproteinases. Our recent studies showed that the degeneration in injury-related cartilage can be prevented in a test tube by the administration of tissue inhibitor of metalloproteinase 1 (TIMP-1). TIMP-1, a natural inhibitor of metalloproteinases, is also known to play an important role in cancer and wound healing of cardiovascular tissues. Taking the advantage of knockout mouse and gene therapy, we currently conduct studies to determine how the lack of TIMP-1 protein can affect the degenerative and repair processes of injured cartilage and whether the increasing TIMP-1 using adenovirus could prevent cartilage degeneration and benefit cartilage repair right after joint injury. In a separate project, we study the differences in cartilage degeneration by mechanical injury and cytokines at the molecular levels and determine the synergic responses between these two factors. This is an important step to understand the mechanisms of initiating osteoarthritis and rheumatoid arthritis, two most common types of arthritis. In addition, I also involved projects to determine 1) functional properties of regenerated cartilage and engineered tissue; 2) cartilage repair using osteochondral graft; and 3) diagnosis of cartilage formation and degeneration using Fourier Transform Infrared Spectroscopy (FTIR) and Magnetic Resonance Imaging (MRI).