The double-labelled sections were imaged using an Olympus AX70 fluorescence microscope and photomicrographs were collected via a high resolution-video camera interfaced with a PC running the ImagePro software (MediaCybernetics, Bethesda, Md.). == Statistical analysis == Inter-group differences in reflectivity, corneal thickness and wavefront aberrations were compared with a paired (or two-sample), two-tailed Student’sttest. SMA-positive myofibroblasts, an effect that was blocked by co-incubation with anti-TGF antibody.In vivo, anti-TGF treatment post-PRK resulted in less SMA immunoreactivity in the sub-ablation stroma, lower corneal reflectivity, less stromal re-growth and lower non-spherical, higher order aberration (HOA) induction than controls. However, there were no inter-group differences in epithelial regeneration or lower order aberration changes. == Conclusions == Anti-TGF treatment reduced feline myofibroblast differentiationin vitroand following PRK. It also decreased corneal haze and fine-grained irregularities in ocular wavefront after PRK, suggesting that attenuation of the differentiation of keratocytes into myofibroblasts can significantly enhance optical quality after refractive surface ablations. Keywords:laser refractive surgery, wavefront aberrations, optical quality, steroids, wound healing, myofibroblasts, keratocytes Increasing awareness of the potential risk of iatrogenic keratectasia after laserin situkeratomileusis (LASIK) has led to a renewed desire for Slc3a2 photorefractive keratectomy (PRK) and prompted the development of advanced surface ablation techniques like laser subepithelial keratomileusis (LASEK)1and Epi-LASIK2. One major disadvantage of surface ablations over LASIK is the more pronounced wound healing response, whose functional consequences include a longer visual rehabilitation period, regression and haze. Since these side effects can significantly limit the treatment of higher myopia (examined in3-5), several attempts have been made to decrease their occurrence through preservation of the epithelial Cefsulodin sodium layer (e.g.LASEK and Epi-LASIK) and pharmacological modulation of wound healing, as proposed in the early days of PRK6. Topical steroids have been used widely7, but their effects on haze and refractive regression remain controversial8-11. Mitomycin C, a cytostatic agent originally launched for chemotherapy of malignant tumors, has also been shown to attenuate wound healing after PRK, particularly in cases with higher susceptibility for regression and haze,i.e.those involving the treatment of higher myopia12-15. However, security issues and side effects have afflicted the use of steroids (elevation of intraocular pressure, cataract induction and delayed epithelial healing) and Mitomycin C (cytotoxic, possibly mutagenic, limited data on long-term keratocyte integrity), prompting the search for alternatives. One means of modulating corneal wound-healing is usually via the inhibition of transforming growth factor (TGF)16,17. TGF is usually a multifunctional cytokine released by the lacrimal gland, the corneal epithelium and conjunctival cells18. TGF Cefsulodin sodium promotes keratocyte proliferation19,20, migration21, differentiation into myofibroblasts that express -smooth muscle mass actin (SMA – examined in22) and the deposition of extracellular matrix proteins19. TGF has been shown to play a crucial role in the development of haze after PRK, so that application of anti-TGF antibodies to the eye reduces both corneal reflectivity (haze) and fibrosis after PRK in rabbits16,17. However, stromal re-growth still occurred, suggesting that at least in the rabbit, stromal regeneration may be controlled by TGF-independent mechanisms17. Cefsulodin sodium Other than haze, the optical effects of blocking TGF after PRK16,17have by no means yet been examined. The cat model used in the present study is unique in allowing simultaneous investigation of biological and optical aspects of corneal wound healing after PRK23-25. However, before screening thein situeffects of anti-TGF treatment in the cat, we first measured the response of feline corneal keratocytes to TGF stimulationin vitro,to verify that they behaved similarly to keratocytes from rabbits, Cefsulodin sodium pigs and humans.In vivoexperiment were then carried out to test the hypothesis that blocking TGF activity in the cat vision after PRK: (1) decreases transformation of corneal keratocytes into contractile myofibroblasts, (2) decreases haze (corneal reflectivity) by reducing the incidence of reflective myofibroblasts in the ablation optical zone, (3) decreases refractive regression by slowing keratocyte proliferation and the generation of new extracellular matrix in the stroma, and (4) decreases the induction of higher order aberrations (HOAs) by.