CDH1 reduces endothelial cell permeability by enhancing CDH5 membrane expression under chronic intermittent hypoxia

Area of Science:

• Cardiovascular Biology
• Cellular Biology
• Pathophysiology

Background:

• Chronic intermittent hypoxia (CIH) is central to obstructive sleep apnea (OSA) pathophysiology.
• Paradoxically, controlled CIH may confer cardiovascular protection.
• Vascular endothelial integrity is crucial for cardiovascular health.

Purpose of the Study:

• To investigate the protective role of E-cadherin (CDH1) in vascular endothelium under CIH.
• To explore CDH1's mechanism in mitigating CIH-induced vascular injury.
• To assess CDH1's potential as a therapeutic target for endothelial dysfunction.

Main Methods:

• Established an endothelial cell model subjected to CIH and oxidized low-density lipoprotein (ox-LDL).
• Utilized immunofluorescence staining to visualize CDH1 and CDH5 expression.
• Assessed endothelial permeability using FITC-dextran assays.

Main Results:

• Under CIH, CDH1 demonstrated a protective effect on endothelial cells.
• CDH1 reduced endothelial permeability by upregulating VE-cadherin (CDH5) at the cell membrane.
• Ox-LDL induced cellular damage, significantly decreasing cell membrane CDH1 expression.

Conclusions:

• CDH1 plays a protective role in vascular endothelial cells against CIH.
• Promoting CDH1 expression may be a novel strategy to reduce vascular injury.
• CDH1 represents a potential therapeutic target for endothelial cell damage.