Moesin expression in fibrosis in the mouse cornea after sterile mechanical trauma or infection.

Abstract

The aim of this study was to compare the expression patterns of 3 important biochemical characteristics of fibrosis-moesin, transforming growth factor (TGF)-β1, and α-smooth muscle actin (SMA) in the mouse cornea with fibrosis induced by common etiologies-sterile mechanical injury and infection. Corneas of 8-week-old C57BL6 mice were either wounded after an anterior keratectomy or were infected by Pseudomonas aeruginosa, and the animals were killed on days 2 and 7, and on weeks 2 and 4 after the procedure. Western blot and immunofluorescence were used to analyze the expression of moesin and phospho-moesin, and the presence of myofibroblasts identified by the expression of α-SMA in the corneal stroma. The expression of TGF-β1 was analyzed by immunofluorescence. By immunofluorescent analysis, TGF-β1, α-SMA, and phospho-moesin were not detected in the normal corneal stroma. However, after either treatment, TGF-β1 expression increased, along with phospho-moesin in the wounded corneal stroma until day 7, and decreased after week 2. No expression of TGF-β1 and phospho-moesin was found at postoperative week 4. Moesin expression increased until week 2. Myofibroblasts positive for α-SMA were detected on day 2 until week 4 and peaked at week 2. Western blot analysis confirmed the immunofluorescent data for moesin, phospho-moesin, and α-SMA. The similar expression pattern of moesin, phospho-moesin, TGF-β1, and α-SMA in the mouse cornea with fibrosis caused by sterile mechanical injury or infection indicated a role for moesin signaling in corneal fibrosis. Interference with the action of moesin may be a potential approach for intervention strategies to avert fibrosis after infection or mechanical injury.