Aspirins effect on skin cells can delay skin repair at wound sites, according to new research in mice that might help lead to development of new treatments.
Aspirin is known to promote bleeding events, and the drug also inhibits wound healing. The researchers findings, published in The Journal of Experimental Medicine, describes how aspirin acts on key skin cells called keratinocytes, delaying skin repair at wound sites. The study used diabetic mice, which are a common model for studying wound healing.
Chronic wounds are a significant public health problem, affecting about 6.5 million people in the U.S. Rising obesity and diabetes rates are contributing to an increase in chronic wounds.
Skin cells called keratinocytes play an important role in wound healing; when keratinocyte migration across the wound is defective, wounds such as diabetic ulcers cannot heal and become chronic wounds. However, researchers do not fully understand how keratinocyte movement during wound healing is regulated.
For the study, scientists from Japan investigated the role of a molecule 12-HHT, which is produced during blood coagulation after a skin injury, and its receptor BLT2, which is found on the surface of keratinocytes. Researchers showed 12-HHT helps to rebuild the epithelial layer at wound sites by aiding the migration of keratinocytes. They also found high-dose aspirin, a commonly used NSAID, delays wound healing by reducing the production of 12HHT.
When researchers used a synthetic mimic of the BLT2 receptor, they found wound healing accelerated in the diabetic mice.
This study describes a novel mechanism for aspirins effect in delaying wound healing and suggests that aspirin should be used with caution in patients with chronic wounds, lead author Takehiko Yokomizo, MD, PhD, said in a news release.
More study is needed to determine whether the best treatment for wound healing might need a combination of BLT2 agonists with growth factors, the authors wrote, adding the study might lead to the possibility of developing drugs to promote healing of chronic wounds in humans.