Erythroid differentiation regulator 1 (Erdr1) enhances wound healing through collagen synthesis in acne skin.

Acne is a chronic skin disease of the pilosebaceous unit resulting from Propionibacterium acnes (P. acnes), a commensal microorganism. Although numerous therapies are available for acne, there is still a need for the development of effective therapies. Erythroid differentiation regulator 1 (Erdr1) has been suggested to be beneficial during inflammatory skin diseases. In the current study, we first showed that Erdr1 expression level was lower in inflammatory acne skin compared to the normal skin, suggesting that Erdr1 was negatively regulated in acne skin. To evaluate the effect of Erdr1 further, Erdr1 was injected subcutaneously in the acne mouse model. Results revealed that the necrotic lesions by inflamed acne were dramatically decreased and collagen synthesis and fibroblasts activation were induced by Erdr1. In addition, Erdr1 reduced the infiltration of inflammatory cells in vivo and accelerated collagen production in P. acnes-treated human dermal fibroblasts through TGF-β/Smad signaling. Taken together, Erdr1 enhanced wound healing through acceleration of collagen synthesis and activation of fibroblasts in acne skin, suggesting its potential use for acne improvement.