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Published on: October 31, 2016
Platelet endothelial cell adhesion molecule-1 (PECAM1) plays a critical role in the maintenance of human vascular
Qi Ren1,2, Limin Ren3, Changjie Ren2
1Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Shandong, China.
Insights
Platelet endothelial cell adhesion molecule-1 (PECAM1) is crucial for maintaining vascular endothelial barrier integrity. Its absence disrupts tight junctions, increasing permeability and contributing to cardiovascular diseases.
Area of Science:
- Cardiovascular Biology
- Endothelial Cell Biology
- Molecular Medicine
Background:
- Cardiovascular endothelial barrier dysfunction is a key factor in numerous cardiovascular diseases.
- Platelet endothelial cell adhesion molecule-1 (PECAM1) is implicated in vascular health.
Purpose of the Study:
- To investigate the role of PECAM1 in maintaining vascular endothelial barrier integrity.
- To elucidate the molecular mechanisms by which PECAM1 influences endothelial barrier function.
Main Methods:
- Utilized human umbilical vein endothelial cells (HUVECs) as an in vitro model for endothelial barrier assessment.
- Employed gene knockdown techniques to study the effects of PECAM1 deficiency.
- Analyzed the formation of tight junction complexes and their associated proteins.
Main Results:
- Knockdown of PECAM1 significantly reduced transendothelial resistance and increased HUVEC monolayer permeability.
- PECAM1 forms a complex with claudin1, occludin, and ESAM, essential for tight junction formation.
- Interleukin-13 exposure reduced PECAM1 expression and impaired endothelial barrier function.
Conclusions:
- PECAM1 is vital for the formation and maintenance of the tight junction complex in endothelial cells.
- PECAM1 deficiency compromises endothelial barrier integrity, potentially contributing to cardiovascular pathologies.
- Targeting PECAM1 may offer therapeutic strategies for cardiovascular diseases associated with barrier dysfunction.
Abstract:
Cardiovascular endothelial barrier dysfunction is associated with a number of cardiovascular diseases. This study aims to investigate the role of platelet endothelial cell adhesion molecule-1 (PECAM1) in the maintenance of the vascular endothelial barrier integrate. Human umbilical vein endothelial cells (HUVECs) were cultured into monolayers using as an in vitro model to assess the endothelial barrier function. Knockdown of the gene of PECAM1 markedly reduced the transendothelial resistance and increased the permeability of the HUVEC monolayers. From the wild HUVECs, we detected a complex of PECAM1, claudin1, occluding and endothelial cell selective adhesion molecule (ESAM); such a complex was not detected in the PECAM1-deficient HUVECs. Knockdown of either claudin1, or occludin, or ESAM, did not affect the formation of the tight junction (TJ) complex. Exposure to recombinant interleukin (IL)-13 inhibited the expression of PECAM1 and down-regulated the HUVEC monolayer barrier function. PECAM1 plays an important role in the formation of TJ complex.
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