Induced myopia in the guinea pig: scleral myofibroblasts and biomechanics

Abstract

Aims: To determine the effect of induced myopia on the in vivo scleral biomechanical properties and scleral cell populations in the guinea pig. Methods: One week old guinea pigs were monocularly deprived of form vision (MD) for 14 days. Cycloplegic refractive error was measured with an IR Optometer, and the results analysed using power vectors and linear mixed modelling. The in vivo ocular biomechanical response was investigated by raising the IOP to 50 mmHg for one hour in anaesthetised animals. A-scan ultrasound measures of axial length were taken every 10 minutes with raised IOP, and after returning IOP to 15 mmHg. The total cell population (DAPI antibody) and myofibroblast population (α-SMA antibody) was determined in transverse scleral sections from the posterior 100 degrees of each eye. Results: The average relative myopic refractive error induced was -4.06 ± 0.35 D, which was mainly the result of vitreous chamber depth (VCD) elongation. This was confirmed by a negative correlation between mean sphere and VCD (R2 = 0.4295). On increasing the IOP the deprived and control eyes showed rapid viscoelastic expansion of the VCD that normal eyes did not show. When the increased IOP was maintained the deprived and control eyes showed lower creep rates than normal eyes. Myofibroblasts were shown to be present in guinea pig sclera, as previously observed in human and tree shrew sclera. On average, approximately 64% of the scleral cells were myofibroblasts. The induction of myopia had minimal effect on the cell populations, except for a decrease in total cell numbers in the 10° region equivalent to the location of scleral crescent formation in myopic human eyes. Conclusions: Ahigh proportion of scleral cells show contractile potential in the guinea pig. Form deprivation appears to minimally affect cell numbers, except in the region equivalent to scleral crescent formation in myopic human eyes. However, the in vivo viscoelastic response of the VCD in deprived eyes differs from that in normal eyes, suggesting some factor(s) other than cell number alone has a role in axial length control.