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. 2008 Jan 23;105(5):1668–1673. doi: 10.1073/pnas.0706315105

Fig. 3.

Fig. 3.

Hypoxia, SDF-1, and CPC differentiation. (A) Akt inhibition (Akt I) of nonactivated and activated CPCs decreased the expression of phospho-Akt, HIF-1α (56% decrease in controls and 44% decrease in GF-treated CPCs), and SDF-1 synthesis. (B) CPCs express CXCR4 at the mRNA and protein levels. The presence of CXCR4 (red) in CPCs was confirmed by immunocytochemistry. (C) Hypoxia up-regulates 16-fold HIF-1α expression in HUVECs. P19CL6 cells were used as positive control. (D) Differentiation and proliferation of nonactivated and activated CPCs. Exposure of activated CPCs to CXCR4 antibody attenuates differentiation in the presence of hypoxia. (E) Expression of HIF-1α in HUVECs transfected with HIF-1α siRNA. When CPCs are cocultured with transfected HUVECs, the differentiation of CPCs into vascular cells decreased as documented by immunocytochemistry. (F) SDF-1 favors CPC differentiation. (G) SDF-1 up-regulates VWF, Mhc11, and Mlc2v in CPCs. Nucleotide sequences are in SI Fig. 10.