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hTCEpi cells stratify, differentiate, and desquamate similar to normal human corneal epithelium. Further study of the hTCEpi cell line may be valuable in studying the molecular mechanisms regulating corneal epithelial cell differentiation and desquamation.

CMTF is a novel, reproducible technique for obtaining epithelial and corneal thickness measurements during clinical in vivo confocal microscopy of the cornea. More importantly, this methodology provides the first objective, quantitative approach for measurement and analysis of depth and thickness of corneal sub-layers which may prove uniquely valuable in temporally assessing corneal function.

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This study confirms our earlier observations that increased corneal light reflectivity following PRK is predominantly due to: (1) distortion of the photoablated stromal surface leading to prominent reflections; and (2) increased reflections from activated and transformed keratocytes. Anti-TGFbeta reduced keratocyte activation and transformation and inhibited stromal fibrosis, leading to a reduction in early light reflectivity as well as to a more rapid decline. Of greatest interest is the unexpected finding that anti-TGFbeta treatment inhibited stromal fibrosis without reducing or delaying post-PRK stromal re-thickening. Based on these findings we propose that corneal thickness may be tightly and dynamically regulated by an unknown, non-TGFbeta mediated pathway. We propose that anti-TGFbeta treatment may be useful in reducing post-PRK corneal haze development in patients by: (1) inhibiting the recruitment of highly reflective, activated keratocytes, (2) inhibiting myofibroblast transformation, and 3) reducing stromal fibrosis.

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