The cornea is exposed to hypoxia under several conditions including sleep, inflammation and wound healing. Being an avascular tissue to maintain transparency, how the cornea homeostatic controls oxygen tension is important. To address this process two models were utilised; a 3D stroma construct of human corneal fibroblasts was stimulated with ascorbate to self-assemble an extracellular matrix, and a corneal organ culture of wounded rat corneas was placed in culture to heal. The models were exposed to normoxic (21%) and hypoxic (1%) and the production of matrix proteins was assessed. The results showed that hypoxia induced a significant decrease in small leucine rich proteoglycans (SLRP) including lumican, decorin and keratocan, a significant increase in perlecan. In the corneal organ culture model wound healing was delayed under hypoxic conditions, due in part to reduced migration and fibronectin deposition. By comparison, there was no difference in type V collagen under hypoxic conditions. Modelling corneal development and repair under conditions of hypoxia show a potential to manipulate conditions to investigate the mechanisms involved.