Studying tissue taken from chronic wounds in humans, the researchers discovered that skin cells get stuck in the middle of the normal healing process and cannot migrate to the wound site. The stalling of the healing process, the researchers discovered, is caused by overabundance of a molecule called c-myc (a product of the ubiquitous myc gene, which has been implicated in many human cancers). This molecule is known to suppress cell migration and to cause the skin to thicken, obstructing reparative cells from reaching the edge of the wound.
The cause of c-myc overproduction was then traced one step up the molecular pathway to beta-catenin, a critical regulator of cell behavior. According to the researchers, beta-catenin activates the production of c-myc as well as other pathways that affect the migration, growth, and regulation of skin cells.
This is the first study to investigate the roles of c-myc and beta-catenin in impairment of wound healing in humans. It is published in the July 1 issue of the American Journal of Pathology.
In normal skin, cells are tightly stuck together in order to create a barrier between the body and the outside world, keeping water in and infections out. But when a wound occurs, skin cells from lower layers loosen from their neighbors and start migrating to the wound site and dividing rapidly. Dr. Tomic-Canic and her colleagues found that in skin with chronic wounds, the cells multiply at a higher rate than usual, yet they are unable to migrate into the wound to close it. Instead, they form thickened layers around the edge, much like a callus or a corn.
Something else also goes awry in chronic wounds, according to the study. As skin cells move upwards, they normally lose their nuclei and form sturdy layers of cross-linked proteins, creating a protective layer over the wound. But in chronic wounds, the researchers found, skin cells are unable to progress to this stage of differentiation, and their nuclei remain present.
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