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Cornea:
doi: 10.1097/ICO.0b013e3181bd45ec
Basic Investigation

Influence of Bilateral Medial Collateral Ligament Injury on mRNA Expression in Distal Corneal Tissues of Control and Ovariohysterectomized Rabbits

Achari, Yamini PhD*; Reno, Carol R*; Morck, Douglas W DVM†; Hart, David A PhD*

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Abstract

Purpose: Corneal tissues are reported to be impacted by physiological changes (eg, menopause), systemic autoimmune diseases, and osteoarthritic-like conditions. In this study, changes in specific mRNA levels in the cornea after a ligament injury in normal and rabbits subjected to surgical menopause were examined.

Methods: Skeletally mature female rabbits were either sham-operated (control) or were subjected to surgical menopause (OVX). Eight weeks post-OVX, subsets of control and OVX animals were subjected to bilateral injuries to their medial collateral ligaments (MCL) of the knee, and 6 and 14 weeks postinjury, corneal tissues were harvested. Using reverse transcriptase-polymerase chain reaction, mRNA levels for several relevant molecules, including matrix molecules, growth factors, cytokines, proteinases, and hormone receptors, were assessed.

Results: mRNA levels for estrogen receptor, decorin, collagens, several growth factors, and inflammatory cytokines decreased in central corneal tissue 6 weeks after distal MCL injury in control animals. The central corneal tissues of animals subjected to OVX alone also exhibited decreases in mRNA levels for a similar set of molecules. When OVX animals were further subjected to MCL injury, the mRNA levels for many of these molecules did not vary from those in the uninjured OVX group. Interestingly, mRNA levels for most molecules were still altered 14 weeks post-MCL injury in the control and OVX animals, a time when the MCL has healed.

Conclusions: Corneal tissues respond to changes resulting from OVX and/or injury. OVX combined with a ligament injury does not appear to have an additive impact on corneal mRNA levels for most of the molecules assessed.

© 2010 Lippincott Williams & Wilkins, Inc.

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