on April 16th, 2015 1 Comment
I have a scar on my chin from a fall I took while rollerskating when I was about 12. One minute I was blithely zooming along to Bob Seger’s hit Against the Wind (earworm alert!), reveling in my new ability to skillfully cross one foot in front of the other and thinking about that cute boy by the snack counter, and the next I was chin down skidding across the flat, grey and (I then realized) very hard floor to come to rest against the wooden wall in an ignominious heap.
Although the experience left an impression on my psyche, as well as my skin, I can’t claim any long-lasting problem from the thin line on my chin. After all, nearly all of us have something similar. But scars can also be debilitating and even dangerous.
Now plastic and reconstructive surgeon Michael Longaker, MD, and pathologist and stem cell expert Irving Weissman, MD, have identified the cell type in mice that is responsible for much of the development of a scar. They’ve shown that blocking this cell’s activity with a small molecule can reduce the degree of scarring. Because a similar drug molecule is already approved for use in humans to treat Type 2 diabetes, the researchers are hopeful that they can begin clinical trials in humans soon. The research was published today in Science.
As Longaker explained in our release on the study:
The biomedical burden of scarring is enormous. About 80 million incisions a year in this country heal with a scar, and that’s just on the skin alone. Internal scarring is responsible for many medical conditions, including liver cirrhosis, pulmonary fibrosis, intestinal adhesions and even the damage left behind after a heart attack.
Longaker and his colleagues found that a subset of a skin cell called a fibroblast is responsible for much of the collagen deposition that leads to scarring. Inhibiting the activity of a protein on the surface of the cells significantly reduced the amount of scarring during wound healing in laboratory mice – from about 30 percent of the original wound area down to about 5 percent -the researchers found. Furthermore, they showed the cells are also involved in the thickening and darkening of skin exposed to radiation therapy for cancer, as well as the spread of melanoma cancer cells in the animals.
Longaker’s been interested in how the skin heals for decades–ever since he learned as a student that, prior to the third trimester, human fetuses heal from trauma or surgery without any scarring. Now he’s excited to learn whether there’s a way to recapture that long-lost ability as adults and at least reduce the degree of scarring during skin repair.
“I’ve been obsessed with scarring for 25 years,” Longaker told me. “Now we’re bringing together the fields of wound healing and tumor development in remarkable new ways. It’s incredibly exciting.”
Longaker and Weissman are both also members of the Stanford Cancer Institute.
Previously: New medicine? A look at advances in wound healing, Stanford-developed device shown to reduce the size of existing scars in clinical trial and Mast cells not required for wound healing, according to Stanford study
Photo by Paulo Alegria