Maintenance of corneal transparency is susceptible to vicious external stimuli, such as trauma. A nicely organized healing cascade is critical for regenerating transparent corneas to avoid vision impairment and to prevent of intraocular infection as well. Healing of stromal incision is characterized by differentiation of corneal stroma keratocytes to fibroblasts and eventually myofibroblasts the latest contribute to scar tissue formation and contraction of stromal extracellular matrix (ECM). Tissue repair-related ECM components are transiently expressed in wound keratocytes/activated fibroblasts/myofibroblasts, epithelial cells, and macrophages.

Lumican is the core protein of one of corneal keratan sulphate proteoglycans, KS-Lum, which regulates collagen fibrillogenesis, e.g., the inter fibril spacing and fibril diameters of stromal collagenous matrixes for the maintenance of corneal stroma transparency [1]. Lumican is also transiently upregulated in an injured corneal epithelium and exhibits a function of wound healing accelerator as a glycoprotein [1]. Moreover, we reported that lumican is critical to epithelial-mesenchymal transformation (EMT) and formation of fibrotic scar tissues in an injured mouse lens [2]. As for the repair in a mesenchymal tissue, lumican plays a critical role in the process of tissue repair in dermis by modulating contractile function of skin fibroblasts [3]. Therefore, we hypothesize that lumican has pivotal roles in the healing of an incision in mouse corneal stroma.

In the present study we investigated the wound healing pattern in corneal stroma following an incision injury in a lumican-null (KO) mouse in comparison to that seen in wild-type (WT) mice. In vitro study of cultured ocular fibroblasts was also performed to uncover the cellular mechanism accountable for delayed in vivo healing of KO corneal stroma.