• Title Professor
  • Education PhD: University of Wisconsin, Madison
  • Office L904
  • Phone 617-358-1235
  • Area of Interest purinoreceptors, EGFR receptors, confocal imaging, wound repair, cell communication and migration

Our laboratory is interested in the response to injury. Injury may be a traumatic event or a change in the integrity of the tissue that occurs from an onset of disease. Our lab uses the cornea to study cell repair as it is a simple model tissue as it is avascular yet highly innervated tissue. In addition, corneal disease and injury remain a major cause of blindness (World Health Organization) and affects over 10 million people worldwide. Diseases such as Type II Diabetes present an overwhelming problem to the cornea with rapid changes in innervation and wound repair. Our lab uses a number of in vitro, organ culture and in vivo models to examine wound repair using a pre-Type II diabetic model. Recently we have shown that changes in the sensory innervation and expression profile in the cornea can occur rapidly and may alter cell communication that underlies collective migration. As the cornea is avascular the wound response is sensitive to soluble factors released with injury that induce downstream signaling events. We speculate that the communication occurs through a family of proteins called pannexins. In addition, the proper repair of the pre-diabetic tissue may be compromised by a family of proteins along the surface of epithelial cells where the polarity of the proteins is misregulated. To determine cell communication after injury we perform high resolution live imaging technologies to examine changes in calcium mobilization, cytoskeletal reorganization and cell motility over time. These are combined with confocal imaging of fluorescent probes in fixed tissues. These are analyzed using a number of MATLAB scripts. These studies require an understanding of the dynamics between matrix molecules and growth factors and how they are released from various depots.

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