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Is PECAM-1 a mechanoresponsive molecule?
K Fujiwara1, M Masuda, M Osawa
1Center for Cardiovascular Research, Department of Medicine, University of Rochester, NY 14624, USA. Keigi_Fujiwara@urmc.rochester.edu
Cell Structure and Function
|May 10, 2001
Summary
Endothelial cells sense fluid shear stress through PECAM-1 (platelet-endothelial cell adhesion molecule-1) located at cell junctions. This interaction triggers a signaling pathway involving tyrosine phosphorylation and ERK activation, suggesting PECAM-1
Area of Science:
- Cell biology
- Biophysics
- Molecular signaling
Background:
- Endothelial cells respond to mechanical stimuli like fluid shear stress.
- The precise molecular mechanisms of endothelial mechanosensing are not fully understood.
- Cell-cell adhesion sites are implicated as potential mechanosensors.
Purpose of the Study:
- To investigate the molecular mechanisms by which endothelial cells sense fluid shear stress.
- To identify key molecules involved in endothelial mechanotransduction.
- To explore the role of PECAM-1 in endothelial cell response to shear stress.
Main Methods:
- Exposure of endothelial cells to physiological levels of fluid shear stress.
- Analysis of tyrosine phosphorylation of cell adhesion molecules.
- Investigation of downstream signaling pathways, including ERK activation.
Main Results:
- PECAM-1 (platelet-endothelial cell adhesion molecule-1), located at interendothelial cell adhesion sites, undergoes tyrosine phosphorylation upon exposure to fluid shear stress.
- PECAM-1 tyrosine phosphorylation initiates a signaling cascade.
- This cascade leads to the activation of ERK (extracellular signal-regulated kinase).
Conclusions:
- The cell-cell adhesion site, specifically PECAM-1, is a critical component in endothelial mechanosensing.
- PECAM-1 tyrosine phosphorylation serves as an early event in the signaling pathway triggered by fluid shear stress.
- PECAM-1 plays a significant role in mediating endothelial cell responses to mechanical forces.