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<p>Chronic intermittent hypoxia (CIH) is the primary pathophysiological basis of obstructive sleep apnea (OSA). However, a certain degree of CIH may enhance vascular stability and protect the cardiovascular system.This study aimed to explore the protective role of CDH1 proteins, known as E-cadherin, on the vascular endothelium under CIH, thereby reducing vascular injury from a novel perspective. An endothelial cell model exposed to CIH and oxidized low-density lipoprotein (ox-LDL) were developed. Immunofluorescence staining and FITC-dextran for endothelial permeability were applied to indicate that under CIH, CDH1 exerts a protective effect on vascular endothelial cells by reducing their permeability through promoting the expression of CDH5, referred to as VE-cadherin, on the cell membrane. In contrast, the damage to cells caused by ox-LDL has led to a notable decrease in the expression of the CDH1 protein on the cell membrane. Therefore, the CDH1 protein may be a novel target for treating vascular endothelial cell injury.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月19日

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  • Jie Zhang,
  • Jihua Zhang,
  • Weiwei Chi,
  • Ying Hao,
  • Chunyan Liu,
  • Dongmei Song,
  • Liping Dong

摘要

Chronic intermittent hypoxia (CIH) is the primary pathophysiological basis of obstructive sleep apnea (OSA). However, a certain degree of CIH may enhance vascular stability and protect the cardiovascular system.This study aimed to explore the protective role of CDH1 proteins, known as E-cadherin, on the vascular endothelium under CIH, thereby reducing vascular injury from a novel perspective. An endothelial cell model exposed to CIH and oxidized low-density lipoprotein (ox-LDL) were developed. Immunofluorescence staining and FITC-dextran for endothelial permeability were applied to indicate that under CIH, CDH1 exerts a protective effect on vascular endothelial cells by reducing their permeability through promoting the expression of CDH5, referred to as VE-cadherin, on the cell membrane. In contrast, the damage to cells caused by ox-LDL has led to a notable decrease in the expression of the CDH1 protein on the cell membrane. Therefore, the CDH1 protein may be a novel target for treating vascular endothelial cell injury.