News Release

Molecular insight into wound healing

Peer-Reviewed Publication

Cold Spring Harbor Laboratory

Scientists have discovered a critical protein involved in skin inflammation. Published in Genes & Development, this study sheds new light on the molecular mechanism of wound healing and identifies a potential new drug target in the treatment of skin disorders like psoriasis.

The epidermis is the fist line of defense against injury and infection. When an injury is incurred, it is usually associated with skin inflammation. Dr. Walter Wahli and colleagues at the University of Lausanne in Basel, Switzerland have determined that the nuclear receptor protein PPARbeta (peroxisome proliferator-activated receptor beta) functions as a critical gene regulator in the cellular response to inflammation.

Upon injury, specialized epidermal cells called keratinocytes receive inflammatory signals that induce keratinocyte differentiation and migration to the site of injury, where they initiate the wound healing process. Dr. Wahli and colleagues have discovered that these inflammatory signals actually promote PPARbeta expression and the PPARbeta protein, in turn, activates the genes responsible for keratinocyte differentiation.

Dr. Wahli found that mice lacking PPARbeta are deficient in wound healing because there are an insufficient number of keratinocytes at the injury site. According to this study, PPARbeta functions by converting the inflammatory signal at the cell surface into an organized pattern of gene expression that enables keratinocytes to respond appropriately to injury.

In addition to wound healing, PPARbeta may be involved in other processes that involve inflammation-induced keratinocyte differentiation, like psoriasis. Further research will delineate the role of PPARbeta in such disorders and determine the utility of PPARbeta from a therapeutic perspective.


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