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Updated: Jun 23, 2026
Phenotypic and Functional Characterization of Endothelial Colony Forming Cells Derived from Human Umbilical Cord Blood
Published on: April 13, 2012
CD34+ and endothelial progenitor cells in patients with various degrees of congestive heart failure
Marco Valgimigli1, Gian Matteo Rigolin, Alessandro Fucili
1University of Ferrara and Cardiovascular Research Center, Salvatore Maugeri Foundation, IRCCS, Gussago, Italy. vlgmrc@unife.it
Insights
Endothelial progenitor cells (EPCs) and CD34(+) cells increase in early heart failure (HF) but decrease in advanced stages, influenced by tumor necrosis factor-alpha (TNF-alpha). This biphasic response highlights changes in regenerative capacity during HF progression.
Area of Science:
- Cardiology
- Regenerative Medicine
- Cell Biology
Background:
- Endothelial progenitor cells (EPCs) and CD34(+) cells are biomarkers of endothelial damage in myocardial infarction.
- Endothelial dysfunction is common in heart failure (HF), but EPC mobilization patterns remain uncharacterized.
- This study investigates EPC and CD34(+) cell dynamics in HF patients.
Purpose of the Study:
- To investigate the mobilization patterns of CD34(+) cells and EPCs in heart failure (HF).
- To correlate these patterns with HF severity and etiological factors.
- To explore the role of inflammatory markers and growth factors in HF-associated EPC changes.
Main Methods:
- Quantified peripheral blood CD34(+) cells and EPCs (colony-forming units) in 91 HF patients and 45 controls.
- Assessed levels of Tumor Necrosis Factor-alpha (TNF-alpha), its receptors, VEGF, SDF-1, G-CSF, and BNP.
- Correlated cell counts with New York Heart Association (NYHA) functional class and disease origin.
Main Results:
- HF patients exhibited increased CD34(+) cells, EPCs, TNF-alpha, VEGF, SDF-1, and BNP compared to controls.
- CD34(+) cell and EPC levels were inversely correlated with NYHA class and TNF-alpha levels.
- Cell counts were lower in NYHA class IV HF patients compared to class I/II and controls.
Conclusions:
- EPC and CD34(+) cell mobilization in HF follows a biphasic pattern: elevated in early stages and depressed in advanced stages.
- The observed pattern may be linked to the myelosuppressive effects of TNF-alpha.
- Disease origin did not significantly influence EPC mobilization in this HF cohort.
Background:
Peripheral blood CD34(+) cells and circulating endothelial progenitor cells (EPCs) increase in myocardial infarction and vascular injuries as a reflection of endothelial damage. Despite the occurrence of endothelial dysfunction in heart failure (HF), no data are available on EPC mobilization in this setting. We investigated the pattern of CD34(+) cells and EPC mobilization during HF and their correlation with the severity and origin of the disease.
Methods And Results:
Peripheral blood CD34(+) cells (n=91) and EPCs (n=41), assessed both as CD34(+) cells coexpressing AC133 and vascular endothelial growth factor (VEGF) receptor-2 and as endothelial colony-forming units, were studied in HF patients (mean age 67+/-11 years) and 45 gender- and age-matched controls. Tumor necrosis factor-alpha (TNF-alpha) and its receptors (sTNFR-1 and sTNFR-2), VEGF, stromal derived factor-1 (SDF-1), granulocyte-colony stimulating factor (G-CSF), and B-type natriuretic peptide were also measured. CD34(+) cells, EPCs, TNF-alpha and receptors, VEGF, SDF-1, and B-type natriuretic peptide were increased in HF. CD34(+) cells and EPCs were inversely related to functional class and to TNF-alpha, being decreased in New York Heart Association class IV compared with class I and II and controls. No role was found for the origin of the disease.
Conclusions:
CD34(+) cells and EPC mobilization occurs in HF and shows a biphasic response, with elevation and depression in the early and advanced phases, respectively. This could be related to the myelosuppressive role of TNF-alpha.
