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Related Experiment Video

Updated: Jul 21, 2026

Quantitation of Endothelial Cell Adhesiveness In Vitro

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.

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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.