Wound healing, Proteolytic degradation of extracellular matrix, Cell adhesion and migration, Tissue engineering and biomaterials, Skin biology, Bioethics, Responsible conduct of research, Research policy
The focus of our laboratory is on understanding the biological mechanisms responsible for delayed healing in chronic wounds. We combine the use of clinical materials, such as wound fluid and tissue, with the powerful tools of cell/molecular biology to discover the mechanisms underlying the pathophysiology of delayed healing. We discovered the degradation of fibronectin in chronic wounds, the activation and over-expression of matrix metalloproteinases (MMP-2; MMP-9) and serine proteases in chronic wound fluid; and identified bacteria capable of secreting proteases that can degrade extracellular matrix substrates important for healing.
Ongoing efforts are directed at studying how cells respond to different environmental conditions that may affect cell migration using an in vitro wound model and dermal equivalent. We are actively pursuing the development of a therapeutic strategy to inhibit proteolytic degradation of extracellular matrix to promote wound healing. Collaborative efforts have been directed at projects on keloids, pressure ulcers, colonizing and infecting bacteria, bacterial proteases, and topical antiseptic agents. More recently our laboratory has also pursued studies of POSS-based nanomaterials to develop cartilage/synovial fluid substitutes and hemostatic agents. Other efforts are directed at bioethics, responsible conduct of research, and science policy.
- BSN East Carolina University, 1978
- MSN East Carolina University, 1980
- PhD University of Texas at Austin, 1986
- NIH Postdoctoral Research Fellow: UT-Southwestern, Dallas, TX; Weill-Cornell Medical College, New York, NY, 1986-1991