Wound Healing Biology
The Wound Healing Biology Group has two main areas of focus. The first
is scarless fetal healing. We have recently described a Sprague-Dawley
rat model for scarless fetal repair and have used this model as a platform
to elucidate the molecular mechanisms that underlie this intriguing phenomenon.
We believe that understanding these mechanisms will allow us to someday
manipulate the adult wound healing process to recapitulate the scarless
phenotype. Furthermore, an understanding of the fetal wound healing mechanisms,
may give us a broader comprehension of scarring/fibrosis in general.
This knowledge could then be applied to all fields of medicine in which
scar-formation can be problematic (e.g. scleroderma, cardiac fibrosis
post-MI, biliary strictures, post-operative peritoneal adhesions).
The second area of interest for the Wound Healing Biology Group is keloid
pathogenesis. Keloids are the result of pathologic over-healing and represent
a worldwide biomedical burden with approximately two billion people at
risk. They are not only aesthetically unattractive, but can result in
functional impairments and physical deformities with many attendant fiscal,
social, and psychological sequelae. At present, there are no effective
biologically based therapies to treat keloids; To this day, we are in
effect treating the symptoms, without addressing the cause of the problem.
We have recently submitted an R01 (June 1, 2001) aimed at understanding
the biology underlying keloid pathogenesis. We intend to approach this
challenge using a novel keratinocyte/fibroblast co-culture system and
the power of microarray technology.
