Disease Models & Mechanisms · 6 authors, 4 centres
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This preclinical mouse study used a novel lineage-tracing model and fibroblast transplantation to show that activated corneal fibroblasts can revert to a keratocan-expressing keratocyte phenotype when relocated to a normal stromal extracellular matrix.
This study investigated the fate of activated corneal fibroblasts after wound healing using a novel I-KeramTmG lineage-tracing mouse model and transplantation of in vitro-expanded fibroblasts. The authors demonstrated that all cells in repaired corneal scars originated from keratocytes. A key finding was that transplanted fibroblasts, which do not express keratocan in vitro, regained keratocan expression (eGFP) in vivo when relocated into a normal corneal stromal niche. This reversion was more robust in early-passage (P1) fibroblasts than in later-passage (P3) cells. The study indicates that the properties of the extracellular matrix, such as stiffness, are crucial in directing this phenotypic plasticity. Limitations include the use of a mouse model, the inability to fully exclude a role for bone marrow-derived cells, and the observation that some fibroblasts, especially expanded myofibroblasts, did not revert. The findings have translational implications for modulating corneal scarring and using decellularized corneas or genetically modified cells for therapy.
