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10:24
Quantitation of Endothelial Cell Adhesiveness In Vitro
Published on: June 18, 2015
Proinflammatory stimuli regulate endothelial hyaluronan expression and CD44/HA-dependent primary adhesion
M Mohamadzadeh1, H DeGrendele, H Arizpe
1Laboratory of Molecular Pathology, Department of Pathology, The University of Texas Southwestern Medical Center, Dallas, Texas 75235-9072, USA.
The Journal of Clinical Investigation
|February 14, 1998
Summary
Inflammation involves leukocyte adhesion to endothelial cells via CD44 and hyaluronan (HA). Pro-inflammatory signals induce HA on microvascular endothelial cells, enhancing leukocyte extravasation during inflammation.
Area of Science:
- Immunology
- Cell Biology
- Vascular Biology
Background:
- Leukocyte extravasation is crucial for inflammatory responses.
- Adhesion molecules like CD44 mediate leukocyte-endothelial cell interactions.
- Regulation of hyaluronan (HA) on endothelial cells is not well understood.
Purpose of the Study:
- Investigate the regulation of endothelial hyaluronan (HA) expression.
- Determine the role of HA in leukocyte adhesion and extravasation.
- Identify factors that induce HA expression on endothelial cells.
Main Methods:
- Utilized cultured endothelial cell lines and primary cultures.
- Stimulated cells with pro-inflammatory cytokines (TNFα, IL-1β) and bacterial lipopolysaccharide.
- Assessed hyaluronan (HA) expression and CD44-dependent adhesion under flow conditions.
Main Results:
- Pro-inflammatory cytokines and lipopolysaccharide induce HA expression on endothelial cells.
- HA inducibility is specific to microvascular endothelial cells.
- Increased HA enhances CD44-mediated leukocyte adhesion.
Conclusions:
- Hyaluronan (HA) is an inducible endothelial adhesion molecule.
- CD44-HA interactions contribute to lymphocyte extravasation at inflammatory sites.
- Cytokine-induced HA expression on endothelial cells facilitates inflammatory cell recruitment.
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