Abstract 13: Documentation Of Improved Ocular Surface Health After Corneal Neurotisation And Reinnervation Using Magnetoencephalography And Histology

RESULTS: In vivo, Fmod mouse wounds representing a lost-of-function model presented markedly increased myofibroblasts after wound closure compared with wild-type (WT) controls. Intradermal injection of FMOD representing gain-of-function models led to significantly decreased myofibroblast accumulation in the wound areas of multiple animal species, including WT mice and Fmod mice, rats and pigs with high-mechanical loading wounds. Moreover, FMOD injection significantly stimulated Il1β expression, which likely contributed to the diminished number of myofibroblasts. In vitro, FMOD alone stimulated myofibroblast (but not fibroblast) apoptosis as effectively as IL1β. Remarkably, even in the presence of TGFβ1 that completely blocked the effect of IL1β, FMOD promoted myofibroblast apoptosis. Meanwhile, IL1 receptor antagonist (IL1RA) fully rescued myofibroblasts from FMOD-induced apoptosis and blocked FMOD-stimulated myofibroblast IL1β expression. Thus, FMOD selectively promoted apoptosis of myofibroblasts but not fibroblasts via an IL1β-dependent pathway.