Stories about: wound healing

How our neutrophils might sabotage wound healing in diabetes

When you get a cut or a scrape, your body jumps into action, mobilizing a complicated array of cells and factors to stem bleeding, keep the wound bacteria-free and launch the healing process.

For most of us, that process is complete in a couple of weeks. But for many people with type 1 and type 2 diabetes, delayed wound healing can have permanent consequences. For example, between 15 and 25 percent of diabetes patients develop chronic foot ulcers. Those ulcers are the root cause of roughly two-thirds of lower limb amputations related to diabetes.

Why don’t these wounds close? Blame a perfect storm of diabetic complications, such as reduced blood flow, neuropathy and impaired signaling between cells. According to research by Denisa Wagner, PhD, of Boston Children’s Hospital’s Program in Cellular and Molecular Medicine, a poorly understood feature of our immune system’s neutrophils may be one more ingredient in the storm.

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Give me some skin (or not)

GROWTH CONTROL: Under conditions of low cell density (top image), Yap1, shown in green, is concentrated in cell nuclei, where it turns on growth-promoting genes. Under conditions of cell crowding (bottom image), Yap1 is kept out of cell nuclei (black areas) and is unable to act. Instead it's spread throughout the cell cytoplasm.

Generating new skin for burn victims and treating skin cancer are two sides of the same coin, according to a new study, which also reveals an inborn “crowd control” mechanism that flips the coin. Healthy people have a switch that senses how tightly cells are packed in the “neighborhood,” and turns growth-promoting genes on or off as needed in epidermal (skin-forming) stem cells.

Fernando Camargo, a researcher in the Children’s Hospital Boston Stem Cell Program, has worked out how this switch works and why it’s stuck “on” in cancers like squamous cell carcinoma, the second most common skin cancer. That could be a fresh clue to treating these cancers.

And as Camargo’s team demonstrated in mice, tinkering with that same switch could grow new skin when it’s needed, to heal a burn or ulcer.

Camargo, born in Peru and named a Pew Scholar last year at the age of 33, has been interested in understanding what maintains organs at a specific size. How do our skin and kidneys and livers “know” when it’s time to stop growing?

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