Figure 3
Figure 3. Hypoxia up-regulates expression of the membrane-bound VEGF-1 receptor from monocytes but not HUVECs. (A) Human peripheral blood monocytes were cultured at ambient O2 or 0.5% O2 in the presence of 100 ng/mL GM-CSF. After 48 hours, cells were analyzed for expression of mVEGFR-1 by flow cytometry. Results from a representative donor are shown. The shaded peak represents the staining of the isotype control. (B) mVEGFR-1 expression was analyzed on human peripheral blood monocytes treated as in panel A. Data are the mean ± SEM of 6 normal donors. (C) Expression of mVEGFR-1 mRNA in monocytes by real-time PCR. Data are mean ± SEM of 6 normal donors. (D) HUVECs were cultured at ambient O2 or 0.5% O2 in the presence of 100 ng/mL GM-CSF, and the surface expression of VEGFR-1 and VEGFR-2 was assessed by flow cytometry. Data are mean ± SEM of 4 independent experiments. *P < .001 versus untreated cells at normoxia. **P < .001 versus all other conditions at the same time point.

Hypoxia up-regulates expression of the membrane-bound VEGF-1 receptor from monocytes but not HUVECs. (A) Human peripheral blood monocytes were cultured at ambient O2 or 0.5% O2 in the presence of 100 ng/mL GM-CSF. After 48 hours, cells were analyzed for expression of mVEGFR-1 by flow cytometry. Results from a representative donor are shown. The shaded peak represents the staining of the isotype control. (B) mVEGFR-1 expression was analyzed on human peripheral blood monocytes treated as in panel A. Data are the mean ± SEM of 6 normal donors. (C) Expression of mVEGFR-1 mRNA in monocytes by real-time PCR. Data are mean ± SEM of 6 normal donors. (D) HUVECs were cultured at ambient O2 or 0.5% O2 in the presence of 100 ng/mL GM-CSF, and the surface expression of VEGFR-1 and VEGFR-2 was assessed by flow cytometry. Data are mean ± SEM of 4 independent experiments. *P < .001 versus untreated cells at normoxia. **P < .001 versus all other conditions at the same time point.

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