Endothelial Progenitor Cells Induce a Phenotype Shift in Differentiated Endothelial Cells towards PDGF/PDGFRβ Axis-Mediated Angiogenesis
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Key result
Human EPC conditioned medium increases endothelial cell migration ~2-fold, partially via PDGFRβ signaling.
- 2.13-fold increase
- P<0.001
Population
Human umbilical vein endothelial cells (HUVEC) and ex vivo cultured aortic rings
Comparison
Conditioned medium from human Endothelial… vs Normoxic conditions, recombinant human PDGF-BB…
Design
Preclinical
Authors
Discussion
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Implication
Does not support clinical use of EPC-conditioned medium; leaves open PDGFRβ as a target for future EPC therapy trials.
Structured PICO
P
Population
In vitro and ex vivo experimental models utilizing human umbilical vein endothelial cells and rat aortic rings to investigate the paracrine angiogenic effects of endothelial progenitor cells.
I
Intervention
Conditioned medium from human Endothelial Progenitor Cells (EPC-CM)
C
Comparator
Normoxic conditions, recombinant human PDGF-BB alone, or inactivation of PDGFRβ
O
Outcome
Angiogenesis (proliferation, migration, and sprouting of vascular structures) and PDGFRβ expression/phosphorylationsurrogate
Main Result
Effect estimate: 2.13-fold increase
Absolute Event Rate: 2.13% vs 1%
p-value: p=<0.001
EPC-conditioned medium induces a pro-angiogenic phenotype in endothelial cells by up-regulating the PDGF/PDGFRβ signaling axis, suggesting a mechanism to enhance EPC-based therapies for ischemic tissue.
Limitations
- The study focused on a single cytokine and its receptor (PDGF-BB/PDGFRβ), and cannot preclude that other factors released by EPCs have similar effects on the endothelium.
Cite This Study
Ballmoos et al. (2010) studied Angiogenesis. Endothelial Progenitor Cell-Conditioned Medium (EPC-CM) vs. Control medium was evaluated on HUVEC migration (2.13-fold increase, p=<0.001). Conditioned medium from human endothelial progenitor cells significantly increased migration of differentiated endothelial cells by 2.13-fold, an effect partially inhibited by inactivation of PDGFRβ.
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