Key result
Over-expression of PDGFR-β in endothelial progenitor cells significantly enhanced PDGF-BB-induced proliferation, migration, and angiogenesis via the PI3K/Akt signaling pathway.
p-value: p=<0.01
Over-expression of PDGFR-β enhances the regenerative functions of endothelial progenitor cells via the PI3K/Akt pathway, suggesting a potential mechanistic target for improving postnatal neovascularization.
May enhance EPC regenerative capacity in preclinical models; leaves open translation to human neovascularization therapies.
The proliferation, migration, and angiogenesis of endothelial progenitor cells (EPCs) play critical roles in postnatal neovascularization and re-endothelialization following vascular injury. Here we evaluated whether the over-expression of platelet-derived growth factor receptor-β (PDGFR-β) can enhance the PDGF-BB-stimulated biological functions of EPCs through the PDGFR-β/phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. We first confirmed the expression of endogenous PDGFR-β and its plasma membrane localization in spleen-derived EPCs. We then demonstrated that the PDGFR-β over-expression in EPCs enhanced the PDGF-BB-induced proliferation, migration, and angiogenesis of EPCs. Using AG1295 (a PDGFR kinase inhibitor), LY294002 (a PI3K inhibitor), and sc-221226 (an Akt inhibitor), we further showed that the PI3K/Akt signaling pathway participates in the PDGF-BB-induced proliferation, migration, and angiogenesis of EPCs. In addition, the PI3K/Akt signaling pathway is required for PDGFR-β over-expression to enhance these PDGF-BB-induced phenotypes.
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Wang et al. (2012) studied Vascular injury (in vitro model). PDGFR-β over-expression and PDGF-BB stimulation vs. Empty vector transfection (pEGFP-N2) or untransfected cells was evaluated on EPC proliferation, migration, and angiogenesis (p=<0.01). Over-expression of PDGFR-β in endothelial progenitor cells significantly enhanced PDGF-BB-induced proliferation, migration, and angiogenesis via the PI3K/Akt signaling pathway.
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