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Loss of PECAM-1 function impairs alveolarization
Horace M DeLisser1, Brian P Helmke, Gaoyuan Cao
1Pulmonary, Allergy and Critical Care Division, Department of Medicine, Institute for Medicine and Engineering, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-4318, USA.
The Journal of Biological Chemistry
|December 27, 2005
Summary
Platelet endothelial cell adhesion molecule (PECAM-1) is crucial for lung alveolarization. Inhibiting PECAM-1 function impairs lung development by disrupting septation, not by causing endothelial cell death.
Area of Science:
- Pulmonary Medicine
- Developmental Biology
- Cell Biology
Background:
- Postnatal lung development involves alveolarization, partitioning saccules into smaller air spaces.
- Angiogenesis is implicated in alveolarization, but anti-angiogenic treatments cause endothelial cell death.
Purpose of the Study:
- To investigate the role of platelet endothelial cell adhesion molecule (PECAM-1) in lung alveolarization.
- To determine if inhibiting PECAM-1 function, rather than causing endothelial cell death, impacts lung development.
Main Methods:
- Administered anti-PECAM-1 antibody to neonatal rat pups, inhibiting endothelial cell migration.
- Utilized PECAM-1-null mice to study the effects of PECAM-1 absence on alveolarization.
- Performed three-dimensional lung reconstruction and assessed endothelial cell content, proliferation, and survival.
Main Results:
- Anti-PECAM-1 antibody treatment disrupted alveolar septation in rats, leading to larger airways.
- PECAM-1-null mice exhibited impaired alveolarization without changes in endothelial cell viability.
- Lung endothelial cells from PECAM-1-null mice showed reduced migration.
Conclusions:
- PECAM-1 function is essential for normal postnatal lung development and alveolar septation.
- Inhibiting endothelial cell migration via PECAM-1, unlike causing cell death, effectively inhibits alveolarization.