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K. R. Huxlin, J. Bühren, S. Kenner, L. Nagy, M. Wyble, M. Beha, S. MacRae; Blocking Myofibroblast Differentiation Decreases Higher Order Optical Aberrations After PRK in a Cat Model. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1500. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
To assess whether corneal myofibroblasts are primarily responsible for the post-operative increase in higher order optical aberrations after photorefractive keratectomy (PRK).
Conventional, 10D myopic PRK over a 6mm optical zone was performed on 20 eyes from 10 adult cats under surgical anesthesia. For the first post-operative week, one eye of each cat received 50µL of 1 or 2mg/mL monoclonal mouse anti-TGFß antibody (Clone 1D11, R&D Systems) in Celluvisc (Allergan) twice per day to inhibit keratocyte differentiation into contractile myofibroblasts. Control eyes received Celluvisc solution alone. In eight of the cat eyes, a Shack-Hartmann wavefront sensor was used to collect spot array patterns in the awake-fixating state, before and every 2 wks for 12 wks after PRK. Ocular aberrations were computed up to the 10th order Zernike polynomials for 6mm pupil diameters. Cats were sacrificed 4 or 12 wks post-operatively. Immunohistochemistry was performed on corneal sections to assess expression of α-smooth muscle actin (αSMA), a myofibroblast marker.
Pre-operatively, treated and control eyes possessed similar amounts of defocus (treated: -0.31+0.15D; control: -0.78+0.45D) and higher order aberrations (treated HORMS: 0.33+0.39µm; control HORMS: 0.33+0.09µm). A peak defocus shift to 5.3+1.5D was noted in treated eyes one month after PRK, while control eyes only attained 3.0+0.5D. Control eyes exhibited their greatest HORMS (1.9+0.1µm) 3 wks after PRK, but this decreased to 1.0+0.7µm by 8wks post-op. In contrast, the HORMS of anti-TGFß-treated eyes remained relatively stable throughout the post-operative period examined, hovering between 0.7 and 1.0µm. Control corneas were strongly positive for αSMA 4 wks after PRK, while αSMA expression was absent in anti-TGFß-treated corneas. By 12wks post-op, neither treated nor control eyes exhibited significant αSMA expression.
Anti-TGFß treatment of cat eyes following PRK increased the amount of refractive correction attained while reducing by half the amount of higher order aberrations induced by the surgery. However, this effect was not permanent, peaking 4wks after PRK. This peak optical benefit coincided with a significant reduction in the expression of αSMA in the sub-ablation stroma, suggesting a likely causal relationship between these two phenomena. Our results show for the first time that reactive myofibroblasts, by contracting the cornea, may be partially responsible for the early induction of higher order optical aberrations after PRK.
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