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Endothelial cell adhesion molecule expression in gene-targeted mice
M J Eppihimer1, J Russell, D C Anderson
1Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport 71130-3932, USA.
The American Journal of Physiology
|November 15, 1997
Summary
Gene deficiency in adhesion molecules like ICAM-1 alters E-selectin expression in various tissues. Lack of CD11/CD18 amplifies P-selectin response to TNF-alpha, impacting leukocyte recruitment.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- Leukocyte recruitment is crucial in inflammation and tissue injury.
- Adhesion molecules on leukocytes and endothelial cells mediate this process.
- Gene-targeted mice are vital for studying these molecules' roles.
Purpose of the Study:
- To investigate how deficiencies in CD11/CD18, ICAM-1, or P-selectin affect E- and P-selectin expression.
- To understand the interplay between different adhesion molecules in inflammatory responses.
Main Methods:
- Utilized gene-targeted mice deficient in CD11/CD18, ICAM-1, or P-selectin.
- Employed a dual-radiolabeled monoclonal antibody technique to quantify E- and P-selectin.
- Administered tumor necrosis factor-alpha (TNF-alpha) to induce expression.
Main Results:
- ICAM-1 deficiency elevated basal E-selectin in stomach, large intestine, and brain.
- CD11/CD18 deficiency enhanced P-selectin upregulation following TNF-alpha stimulation.
- E-selectin expression in the brain was reduced in ICAM-1 and P-selectin deficient mice upon TNF-alpha stimulation.
Conclusions:
- Chronic deficiency of certain leukocyte adhesion molecules alters basal and induced expression of other endothelial adhesion molecules.
- This highlights a complex regulatory network among adhesion molecules in inflammation.
- Findings provide insights into molecular mechanisms of leukocyte recruitment and inflammatory diseases.