Annexin A1 mimetic peptide Ac2-26 attenuates mechanical injury induced corneal scarring and inflammation.

Annexin A1 (AnxA1) has been shown to exert potent anti-inflammatory and anti-fibrotic activities in a range of systemic inflammatory disorders. Corneal scarring is characterized by myofibroblast differentiation and disorganized extracellular matrix deposition. This study was aim to explore the potential therapeutic properties of Ac2-26, a mimetic peptide of AnnexinA1 (AnxA1), on TGF-β induced human corneal myofibroblast differentiation and mechanical injury-induced mouse corneal haze. The results found that Ac2-26 treatment dose dependently reduced α-SMA level and other fibrogenic gene expressions in HTK cells stimulated by exogenous TGF-β1. While this anti-fibrotic effect was abolished by an FPR2/ALX inhibitor WRW4. In mice, topical Ac2-26 application suppressed the development of corneal scarring, inhibited myofibroblast differentiation, while promoted the corneal epithelial wound healing. Moreover, Ac2-26 treatment inhibited Ly6G + neutrophil infiltration and reduced corneal inflammatory response. The results provided in vivo and in vitro supports the anti-fibrotic and anti-inflammatory effects of AnxA1 derived peptide Ac2-26, and suggest that AnxA1 mimetic agents might be a promising strategy for the treatment of corneal scarring. • Ac2-26 inhibits myofibroblast differentiation in HTK cells via FPR2. • Topical Ac2-26 attenuated corneal scarring formation and inflammatory response in vivo. • AnxA1 mimetic agents might be a promising strategy for the treatment of corneal fibrosis. [ABSTRACT FROM AUTHOR]