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Published on: July 10, 2018
Moesin expression in fibrosis in the mouse cornea after sterile mechanical trauma or infection
Hong-Y Zhu1, Jennifer Ng, Shuhaida M Salleh
1*Singapore Eye Research Institute, Singapore, Singapore; and †SRP Neuroscience and Behavioral Disorders, Duke-NUS, Singapore, Singapore.
Purpose:
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.
Methods:
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.
Results:
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.
Conclusions:
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.
Insights
Moesin, transforming growth factor-β1 (TGF-β1), and α-smooth muscle actin (SMA) expression patterns were similar in mouse corneas after mechanical injury or infection. This suggests moesin signaling plays a role in corneal fibrosis.
Area of Science:
- Ophthalmology
- Cell Biology
- Biochemistry
Background:
- Corneal fibrosis is a significant cause of vision impairment.
- Understanding the molecular mechanisms underlying corneal fibrosis is crucial for developing effective treatments.
- Key proteins like moesin, TGF-β1, and α-SMA are implicated in fibrotic processes.
Purpose of the Study:
- To compare the expression patterns of moesin, TGF-β1, and α-SMA in mouse corneas following sterile mechanical injury or Pseudomonas aeruginosa infection.
- To investigate the role of moesin signaling in the development of corneal fibrosis.
Main Methods:
- Induction of corneal fibrosis in C57BL6 mice via mechanical injury (keratectomy) or bacterial infection (P. aeruginosa).
- Analysis of protein expression (moesin, phospho-moesin, TGF-β1, α-SMA) at various time points (days 2, 7; weeks 2, 4) using Western blot and immunofluorescence.
- Identification of myofibroblasts through α-SMA expression.
Main Results:
- TGF-β1, α-SMA, and phospho-moesin were upregulated in wounded corneas, peaking by day 7 and decreasing by week 4.
- Moesin expression increased up to week 2.
- α-SMA positive myofibroblasts were present from day 2 to week 4, with a peak at week 2.
- Similar expression patterns were observed for both injury types.
Conclusions:
- Moesin, TGF-β1, and α-SMA exhibit similar expression patterns in response to both mechanical injury and infection, suggesting a common fibrotic pathway.
- Moesin signaling is implicated in the pathogenesis of corneal fibrosis.
- Targeting moesin action may offer a therapeutic strategy to prevent corneal fibrosis.
