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An X-Ray Diffraction Study of Corneal Structure in Mimecan-Deficient Mice

¹From the Structural Biophysics Group, School of Optometry and Vision Sciences, and the ²Cardiff Institute of Tissue Engineering and Repair, Cardiff University, Cardiff, Wales, United Kingdom; and the ³Division of Biology, Kansas State University, Manhattan, Kansas.

PURPOSE. Keratan sulfate proteoglycans (KSPGs) in the corneal stroma are believed to influence collagen fibrillar arrangement. This study was performed to investigate the fibrillar architecture of the corneal stroma in mice homozygous for a null mutation in the corneal KSPG, mimecan.

METHODS. Wild-type (n = 9) and mimecan-deficient (n = 10) mouse corneas were investigated by low-angle synchrotron x-ray diffraction to establish the average collagen fibrillar spacing, average collagen fibril diameter, and level of fibrillar organization in the stromal array.

RESULTS. The mean collagen fibril diameter in the corneas of mimecan-null mice, as an average throughout the whole thickness of the tissue, was not appreciably different from normal (35.6 ± 1.1 nm vs. 35.9 ± 1.0 nm). Average center-to-center collagen fibrillar spacing in the mutant corneas measured 52.6 ± 2.6 nm, similar to the 53.3 ± 4.0 nm found in wild-type mice. The degree of local order in the collagen fibrillar array, as indicated by the height-width (H:W) ratio of the background-subtracted interfibrillar x-ray reflection, was also not significantly changed in mimecan-null corneas (23.4 ± 5.6), when compared with the corneas of wild-types (28.2 ± 4.8).

CONCLUSIONS. On average, throughout the whole depth of the corneal stroma, collagen fibrils in mimecan-null mice, unlike collagen fibrils in lumican-null mice and keratocan-null mice, are of a normal diameter and are normally spaced and arranged. This indicates that, compared with lumican and keratocan, mimecan has a lesser role in the control of stromal architecture in mouse cornea.

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