biostudies-literature00530Chandler HLU.S. Department of Health & Human Services | NIH | National Institute of General Medical SciencesNIDDK NIH HHSNIA NIH HHSNHLBI NIH HHSU.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin DiseasesU.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood InstituteNIAMS NIH HHSNIGMS NIH HHSU.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases71https://www.ebi.ac.uk/biostudies/studies/S-EPMC6382791biostudies-literatureUnknown2The cornea plays an important role in transmitting light and providing protection to the eye, but is susceptible to injury and infection. Standard treatments for corneal wounds include topical lubricants, antibiotics, bandage contact lens, and surgery. However, these measures are often ineffective. Here we show that MG53, a protein with an essential role in cell membrane repair, contributes to the corneal injury-repair process. Native MG53 is present in the corneal epithelia, tear film, and aqueous humor, suggesting its potential function in corneal homeostasis. Knockout of MG53 in mice causes impaired healing and regenerative capacity following injury. Exogenous recombinant human MG53 (rhMG53) protein protects the corneal epithelia against mechanical injury and enhances healing by promoting migration of corneal fibroblasts. Using in vivo alkaline-induced injury to the rat cornea, we show that rhMG53 promotes re-epithelialization and reduces post-injury fibrosis and vascularization. Finally, we show that rhMG53 modulates TGF-β-mediated fibrotic remodeling associated with corneal injury. Overall, our data support the bi-functional role of MG53 in facilitating corneal healing and maintaining corneal transparency by reducing fibrosis and vascularization associated with corneal injuries.Communications biologyMG53 promotes corneal wound healing and mitigates fibrotic remodeling in rodents.PMC6382791DK106394GM123887R44 GM123887R44 DK112403AG056919R01 HL124122HL124122DK112403R01 DK106394R01 AR061385AR070752R43 GM123887R01 AR067766AR067766AR061385R01 AG056919R01 AR070752Chandler HLAdesanya TMAKaili DJiang QZhu HPeterson CMWYang CWehrman RFZhou XGeng BWang QTan TMa JYi FGemensky-Metzler AJ53falseMG53 promotes corneal wound healing and mitigates fibrotic remodeling in rodents.The cornea plays an important role in transmitting light and providing protection to the eye, but is susceptible to injury and infection. Standard treatments for corneal wounds include topical lubricants, antibiotics, bandage contact lens, and surgery. However, these measures are often ineffective. Here we show that MG53, a protein with an essential role in cell membrane repair, contributes to the corneal injury-repair process. Native MG53 is present in the corneal epithelia, tear film, and aqueous humor, suggesting its potential function in corneal homeostasis. Knockout of MG53 in mice causes impaired healing and regenerative capacity following injury. Exogenous recombinant human MG53 (rhMG53) protein protects the corneal epithelia against mechanical injury and enhances healing by promoting migration of corneal fibroblasts. Using in vivo alkaline-induced injury to the rat cornea, we show that rhMG53 promotes re-epithelialization and reduces post-injury fibrosis and vascularization. Finally, we show that rhMG53 modulates TGF-β-mediated fibrotic remodeling associated with corneal injury. Overall, our data support the bi-functional role of MG53 in facilitating corneal healing and maintaining corneal transparency by reducing fibrosis and vascularization associated with corneal injuries.2019-01-01T00:00:00Z20192024-10-17T14:18:23.738Z2019-08-04T07:36:34ZS-EPMC63827913079304910.1038/s42003-019-0316-7