Wound healing is a complex process that is dependent on the restoration of the epithelial layer, the outermost layer of the skin, over the wound surface. Skin cells called keratinocytes play an important role in this process; when keratinocyte migration across the wound is defective, wounds such as diabetic ulcers cannot heal and become chronic wounds. However, we do not fully understand how keratinocyte movement during wound healing is regulated.
Researchers from Japan investigated the role of a molecule called 12-HHT and its receptor BLT2 in wound healing; 12-HHT is produced during blood coagulation following skin injury and BLT2 is found on the surface of keratinocytes. The researchers showed that 12-HHT promotes the re-formation of the epithelial layer at wound sites by enhancing the migration of keratinocytes. They discovered that high dose aspirin, the most commonly used nonsteroidal anti-inflammatory drug, delays wound healing by reducing the production of 12-HHT. The researchers also found that a synthetic mimic of BLT2 accelerated wound healing in diabetic mice (a model that is commonly used to investigate delayed wound healing).
Lead author Takehiko Yokomizo stated that, "This study describes a novel mechanism for aspirin's effect in delaying wound healing and suggests that aspirin should be used with caution in patients with chronic wounds."
Further work will be required to establish whether optimal treatment for wound healing might require a combination of approaches, such as BLT2 agonists together with growth factors to promote the number of wound-healing cells at the wound site.
Researchers showed that 12-HHT promotes the re-formation of the epithelial layer at wound sites by enhancing the migration of keratinocytes
High dose aspirin, the most commonly used nonsteroidal anti-inflammatory drug, delays wound healing by reducing the production of 12-HHT
Aspirin should be used with caution in patients with chronic wounds
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