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Updated: Dec 21, 2025
A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
Published on: July 14, 2016
Involvement of moesin phosphorylation in ischemia/reperfusion induced inner blood-retinal barrier dysfunction
Jing Xu1, Qiong Liu1, Ming Ma1
1Department of Ophthalmology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong Province, China.
Aim:
To investigate the role of moesin and its underlying signal transduction in retinal vascular damage induced by retinal ischemia-reperfusion (RIR) insult.
Methods:
C57BL/6 mice were subjected to continued ischemia for 45min, followed by blood reperfusion. The expression and phosphorylation of moesin in retinal vessels were detected by immunohistochemistry and Western blotting. The inner blood-retinal barrier was evaluated using FITC-dextran leakage assay on whole-mount retina. Further studies were conducted to explore the effects of p38 mitogen-activated protein kinase (MAPK) pathway on the involvement of moesin in RIR-evoked retinal vascular hyperpermeability response.
Results:
It revealed that RIR induced moesin phosphorylation in a time-dependent manner after reperfusion. The phosphorylation of moesin was alleviated by inhibitions of p38 MAPK, while this treatment also ameliorated the dysfunction of inner blood-retinal barrier.
Conclusion:
The results suggest that moesin is involved in RIR-evoked retinal vascular endothelial dysfunction and the phosphorylation of moesin is triggered via p38 MAPK activation.
Insights
Retinal ischemia-reperfusion injury activates moesin phosphorylation via the p38 MAPK pathway, contributing to retinal vascular damage. Inhibiting this pathway protects the inner blood-retinal barrier.
Area of Science:
- Ophthalmology
- Vascular Biology
- Cell Signaling
Background:
- Retinal ischemia-reperfusion (RIR) insult causes significant retinal vascular damage.
- Understanding the molecular mechanisms underlying RIR-induced vascular dysfunction is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the role of moesin in retinal vascular damage following RIR.
- To elucidate the signal transduction pathways, specifically the p38 MAPK pathway, involved in moesin activation during RIR.
Main Methods:
- C57BL/6 mice underwent 45 minutes of retinal ischemia followed by reperfusion.
- Moesin expression and phosphorylation were assessed using immunohistochemistry and Western blotting.
- Inner blood-retinal barrier integrity was evaluated via FITC-dextran leakage assay.
- The impact of p38 MAPK inhibition on moesin phosphorylation and vascular permeability was examined.
Main Results:
- RIR induced a time-dependent increase in moesin phosphorylation post-reperfusion.
- Inhibition of p38 MAPK significantly reduced moesin phosphorylation.
- Blocking the p38 MAPK pathway also ameliorated inner blood-retinal barrier dysfunction.
Conclusions:
- Moesin plays a critical role in RIR-induced retinal vascular endothelial dysfunction.
- Phosphorylation of moesin is a key event triggered by p38 MAPK activation in response to RIR.
- Targeting the p38 MAPK/moesin pathway may offer a therapeutic approach for RIR-related retinal vascular injury.
