Delayed wound healing is a major problem in patients with diabetes, which significantly impairs their quality of life. Prostaglandin (PG) D₂ is a major inflammatory lipid mediator synthesized by hematopoietic PGD₂ synthase (HPGDS) from PGH₂, a common precursor of all of PGs. We have previously shown that HPGDS produced PGD₂ is involved in delayed wound healing in diabetic skin. In this study, we investigated the involvement of DP1 receptor in cutaneous wound healing in streptozotocin (STZ)-induced diabetic mice. C57BL/6 mice were injected intraperitoneal with 50 mg/kg of STZ daily for 5 days. Four weeks after the injection of STZ, a full thickness wound was created with an 8-mm diameter biopsy punch on the dorsal of mice. Wound healing was significantly decelerated in diabetic mice compared with non-diabetic mice. HPGDS mRNA was significantly increased in diabetic mouse skin compared to nondiabetic mouse skin. On the other hand, there was no significant change in the amount of DP1 receptor mRNA. Furthermore, immunohistochemically analysis revealed that HPGDS was expressed in epidermal Langerhans cells of diabetic mice, and the DP1 receptor was expressed in keratinocytes. These results suggest that in hyperglycemic skin, PGD₂ produced by Langerhans cells acts on DP1 receptors on keratinocytes and may be involved in delayed wound healing.