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A Methodological Approach to Non-invasive Assessments of Vascular Function and Morphology
Published on: February 7, 2015
Impaired endothelial progenitor cell function predicts age-dependent carotid intimal thickening
Stefanie Keymel1, Christoph Kalka, Tienush Rassaf
1Medical Clinic I, Dept. of Medicine, Division of Cardiology, Pulmonology, and Vascular Medicine, RWTH University Hospital Aachen, Pauwelstrasse 30, 52074, Aachen, Germany.
Basic Research in Cardiology
|August 16, 2008
Summary
Endothelial progenitor cell (EPC) function, not number, predicts age-related vascular changes like intima-media thickness. Impaired EPC function accelerates arterial thickening, highlighting its role in vascular remodeling.
Area of Science:
- Cardiovascular Biology
- Vascular Biology
- Cellular Aging
Background:
- Age-related endothelial dysfunction is linked to qualitative, not quantitative, changes in endothelial progenitor cells (EPCs).
- Animal models suggest impaired EPC function accelerates arterial intimal thickening.
Purpose of the Study:
- To determine if qualitative or quantitative alterations in endothelial progenitor cells (EPCs) predict age-related structural changes in vessel walls.
- To investigate the relationship between EPC function and intima-media thickness (IMT).
Main Methods:
- Measured intima-media thickness (IMT) in the common carotid artery of younger and older healthy adults.
- Quantified circulating endothelial progenitor cells (EPCs) using flow cytometry (KDR(+)/CD34(+) and KDR(+)/CD133(+)).
- Assessed ex vivo EPC function, including chemotaxis, proliferation, and survival.
Main Results:
- Older subjects exhibited significantly thicker IMT compared to younger subjects.
- Significant inverse correlations were found between IMT and EPC chemotaxis and survival, but not EPC numbers.
- Multivariate analysis identified age, mean arterial pressure, and EPC migration as independent predictors of IMT.
Conclusions:
- Impaired endothelial progenitor cell (EPC) function contributes to accelerated vascular remodeling.
- This suggests a mechanism for age-related structural vessel wall changes due to chronic endothelial maintenance issues.
