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Analysis of Physiologic E-Selectin-Mediated Leukocyte Rolling on Microvascular Endothelium
Published on: February 11, 2009
Stiff substrates enhance monocytic cell capture through E-selectin but not P-selectin
Joanna L MacKay1, Daniel A Hammer
1Department of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104, USA.
Insights
Vascular stiffening may enhance inflammatory cell adhesion via E-selectin, but not P-selectin. This finding suggests a role for arterial stiffness in promoting leukocyte recruitment in inflammatory diseases.
Area of Science:
- Biomedical Engineering
- Immunology
- Cardiovascular Biology
Background:
- Vascular stiffening is linked to inflammatory diseases like atherosclerosis, diabetes, and obesity.
- Leukocyte recruitment into tissues drives these diseases, but the role of vascular stiffness is unclear.
Purpose of the Study:
- To investigate if leukocyte capture from blood flow is enhanced on stiffer substrates.
- To model in vitro blood flow and measure monocytic cell adhesion to E-selectin and P-selectin under varying stiffness conditions.
Main Methods:
- Perfusion of monocytic cells over hydrogels mimicking healthy and diseased artery stiffness.
- Hydrogels coated with endothelial adhesion proteins E-selectin or P-selectin.
- Quantification of cell attachment, duration, and rolling velocity.
Main Results:
- Cell attachment to P-selectin was independent of substrate stiffness.
- Attachment to E-selectin was enhanced on stiffer gels.
- Cells attached in greater numbers, for longer durations, and rolled slower on stiff E-selectin coated gels.
Conclusions:
- Vascular stiffening may promote leukocyte adhesion via E-selectin.
- The effect of vascular stiffening on leukocyte adhesion is dependent on the specific adhesion molecule involved.
- Arterial stiffness could contribute to leukocyte recruitment in inflammatory conditions where E-selectin is present.
Abstract:
The stiffening of blood vessel walls is associated with inflammatory diseases, including atherosclerosis, diabetes, and obesity. These diseases are driven by the excessive recruitment of inflammatory leukocytes out of the bloodstream and into tissues, but whether vascular stiffening plays a direct role in this process is not clear. In this study, we investigated the possibility that leukocyte capture from blood flow is enhanced on stiffer substrates. We modeled blood flow in vitro by perfusing monocytic cells over hydrogels that matched the stiffness of healthy and diseased arteries. The hydrogels were coated with either E-selectin or P-selectin, which are the endothelial adhesion proteins known to mediate immune cell capture from flow. Interestingly, we discovered that cell attachment to P-selectin coated gels was not dependent on substrate stiffness, while attachment through E-selectin was enhanced on stiffer gels. Specifically we found that on E-selectin coated gels, cells attached in greater numbers, remained attached for longer time periods, and rolled more slowly on stiff gels than soft gels. These results suggest that vascular stiffening could promote leukocyte adhesion to vessel walls where E-selectin is expressed, but may have less of an effect when P-selectin is also present.
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