Lack of transient receptor potential ankyrin 1 (TRPA1) retards cutaneous wound healing in mice: A preliminary study

Wound healing is an important process in various diseases, and elucidating the underlying mechanism is essential for developing therapeutic strategies. We investigated whether the loss of transient receptor potential ankyrin 1 (TRPA1) affects the cutaneous wound healing process in mice. We assessed the formation of granulation tissue by myofibroblasts and macrophages, re-epithelialization, and related gene expression. TRPA1-null (KO) and wild-type (WT) C57BL/6 mice were used for establishing the wound model. Two round full-thickness excision wounds (diameter, 5.0 mm) were produced in the dorsal skin of mice under general anesthesia. After specific intervals, healing was evaluated using macroscopic observation, histology, immunohistochemistry, and real-time reverse transcription-polymerase chain reaction (RT-PCR). TRPA1 KO retarded the formation of granulation tissue and re-epithelialization in the healing of cutaneous wound. Furthermore, TRPA1 KO suppressed the appearance of myofibroblasts, macrophage infiltration, and mRNA expression of αSMA, F4/80, and Col-1α2. These findings indicate that TRPA1 is required for cutaneous wound healing in mice. The lack of TRPA1 retards macrophage infiltration and the subsequent fibrotic tissue formation, which might further impair the fibrogenic behavior of fibroblasts.